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<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HIRA establishes greater telomeric chromatin accessibility after ATRX-DAXX loss</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">Deposition of new H3.3 by HIRA-UBN restricts telomeric ssDNA and TERRA R-loops</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">Unresolved TERRA R-loops block new H3.3 deposition by HIRA-UBN</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">CHK1 phosphorylation of H3.3 is critical to prevent ssDNA and TERRA R-loop buildup</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">Inactivating mutations in chromatin modifiers, like the α-thalassemia/mental retardation, X-linked (ATRX)-death domain-associated protein (DAXX) chromatin remodeling/histone H3.3 deposition complex, drive the cancer-specific alternative lengthening of telomeres (ALT) pathway. Prior studies revealed that HIRA, another histone H3.3 chaperone, compensates for ATRX-DAXX loss at telomeres to sustain ALT cancer cell survival. How HIRA rescues telomeres from the consequences of ATRX-DAXX deficiency remains unclear. Here, using an assay for transposase-accessible chromatin using sequencing (ATAC-seq) and cleavage under targets and release using nuclease (CUT&RUN), we establish that HIRA-mediated deposition of new H3.3 maintains telomeric chromatin accessibility to prevent the detrimental accumulation of nucleosome-free single-stranded DNA (ssDNA) in ATRX-DAXX-deficient ALT cells. We show that the HIRA-UBN1/UBN2 complex deposits new H3.3 to prevent TERRA R-loop buildup and transcription-replication conflicts (TRCs) at telomeres. Furthermore, HIRA-mediated H3.3 incorporation into telomeric chromatin links productive ALT to the phosphorylation of serine 31, an H3.3-specific amino acid, by Chk1. Therefore, we identify a critical role for HIRA-mediated H3.3 deposition that ensures the survival of ATRX-DAXX-deficient ALT cancer cells.</div>
</section>
<section id="graphical-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name"></h2>
</section>',
'date' => '2024-11-26',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01315-9',
'doi' => '10.1016/j.celrep.2024.114964',
'modified' => '2024-11-12 09:41:40',
'created' => '2024-11-12 09:41:40',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 3 => array(
'id' => '5065',
'name' => 'Enhancing single-cell ATAC sequencing with formaldehyde fixation, cryopreservation, and multiplexing for flexible analysis',
'authors' => 'Tobias Hohl et al.',
'description' => '<p><span>The assay for transposase-accessible chromatin using sequencing (ATAC-seq) revolutionized the field of epigenetics since its emergence by providing a means to uncover chromatin dynamics and other factors affecting gene expression. The development of single-cell (sc) applications in recent years led to an even deeper understanding of cell type specific gene regulatory mechanisms. One of the major challenges while running ATAC-seq experiments, bulk or sc, is the need for freshly collected cells for successful experiments. While various freezing methods have already been tested and established for bulk and sc ATAC-seq, quality metrics for preserved cells are rather poor or dependent on sampling time when compared to fresh samples. This makes it difficult to conduct all sorts of complex experiments i.e. with multiple conditions, patients, or time course studies. Especially, accounting for batch effects can be difficult if samples need to be processed at different time points of collection. We tackled this issue by adding a fixation step prior to the freezing method. The additional fixation step improved library quality and yield data comparable to fresh samples. The workflow was also tested on multiplexed sc ATAC experiments, set-up for cost-efficient low input sample handling. Sample cross-in, typically encountered in Tn5-based multiplex approaches, were tackled with a computational procedure specifically developed for this approach.</span></p>',
'date' => '2024-11-21',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.11.20.624480v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.11.20.624480',
'modified' => '2025-02-27 10:48:39',
'created' => '2025-02-27 10:48:39',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 4 => array(
'id' => '5055',
'name' => 'On the identification of differentially-active transcription factors from ATAC-seq data',
'authors' => 'Felix Ezequiel Gerbaldo et al.',
'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (a chromVAR-limma workflow with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs—in our case NFkB—at the protein level.</span></p>',
'date' => '2024-10-23',
'pmid' => 'https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1011971',
'doi' => 'https://doi.org/10.1371/journal.pcbi.1011971',
'modified' => '2025-02-26 17:05:52',
'created' => '2025-02-26 17:05:52',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 5 => array(
'id' => '4985',
'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
'authors' => 'Alessia Bagattin et al.',
'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HNF1β mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1β partner, mediates mitosis-specific interaction with TOP1</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1β recruits TOP1 and induces DNA relaxation around bookmarked HNF1β sites</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1β mutation, found in MODY patients, disrupts the interaction with TOP1</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">HNF1β (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that HNF1β remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1β-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1β and TOP1, where a mutation, found in “maturity onset diabetes of the young” patients, disrupts their interaction. Importantly, HNF1β recruits TOP1 and induces DNA relaxation around HNF1β mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1β reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
'date' => '2024-10-08',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
'doi' => '10.1016/j.celrep.2024.114805',
'modified' => '2024-10-14 09:04:44',
'created' => '2024-10-14 09:04:44',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 6 => array(
'id' => '5056',
'name' => 'Rhabdomyosarcoma fusion oncoprotein initially pioneers a neural signature in vivo',
'authors' => 'Jack Kucinski et al.',
'description' => '<p><span>Fusion-positive rhabdomyosarcoma is an aggressive pediatric cancer molecularly characterized by arrested myogenesis. The defining genetic driver, PAX3::FOXO1, functions as a chimeric gain-of-function transcription factor. An incomplete understanding of PAX3::FOXO1’s in vivo epigenetic mechanisms has hindered therapeutic development. Here, we establish a PAX3::FOXO1 zebrafish injection model and semi-automated ChIP-seq normalization strategy to evaluate how PAX3::FOXO1 initially interfaces with chromatin in a developmental context. We investigated PAX3::FOXO1’s recognition of chromatin and subsequent transcriptional consequences. We find that PAX3::FOXO1 interacts with inaccessible chromatin through partial/homeobox motif recognition consistent with pioneering activity. However, PAX3::FOXO1-genome binding through a composite paired-box/homeobox motif alters chromatin accessibility and redistributes H3K27ac to activate neural transcriptional programs. We uncover neural signatures that are highly representative of clinical rhabdomyosarcoma gene expression programs that are enriched following chemotherapy. Overall, we identify partial/homeobox motif recognition as a new mode for PAX3::FOXO1 pioneer function and identify neural signatures as a potentially critical PAX3::FOXO1 tumor initiation event.</span></p>',
'date' => '2024-07-16',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.07.12.603270v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.07.12.603270',
'modified' => '2025-02-26 17:07:24',
'created' => '2025-02-26 17:07:24',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 7 => array(
'id' => '5058',
'name' => 'CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly',
'authors' => 'Hanna Schwaemmle et al.',
'description' => '<p><span>The SWI/SNF (or BAF) complex is an essential chromatin remodeler that regulates DNA accessibility at developmental genes and enhancers. SWI/SNF subunits are among the most frequently mutated genes in cancer and neurodevelopmental disorders. These mutations are often heterozygous loss-of-function alleles, indicating a dosage-sensitive role for SWI/SNF subunits in chromatin regulation. However, the molecular mechanisms that regulate SWI/SNF subunit dosage to ensure proper complex assembly remain largely unexplored. We performed a genome-wide CRISPR KO screen, using epigenome editing in mouse embryonic stem cells, and identified </span><em>Mlf2</em><span><span> </span>and<span> </span></span><em>Rbm15</em><span><span> </span>as regulators of SWI/SNF complex activity. First, we show that MLF2, a poorly characterized chaperone protein, regulates a subset of SWI/SNF target genes by promoting chromatin remodeling activity. Next, we find that RBM15, part of the m</span><sup>6</sup><span>A RNA methylation writer complex, controls m</span><sup>6</sup><span>A modifications on specific SWI/SNF mRNAs to regulate protein levels of these subunits. Misregulation of m</span><sup>6</sup><span>A methylation causes overexpression of core SWI/SNF subunits leading to the assembly of incomplete complexes lacking the catalytic ATPase/ARP subunits. These data indicate that targeting modulators of SWI/SNF complex assembly may offer a potent therapeutic strategy for diseases associated with impaired chromatin remodeling.</span></p>',
'date' => '2024-06-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.06.25.600572v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.06.25.600572',
'modified' => '2025-02-26 17:10:53',
'created' => '2025-02-26 17:10:53',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 8 => array(
'id' => '5061',
'name' => 'Clock-dependent chromatin accessibility rhythms regulate circadian transcription',
'authors' => 'Ye Yuan et al.',
'description' => '<p><span>Chromatin organization plays a crucial role in gene regulation by controlling the accessibility of DNA to transcription machinery. While significant progress has been made in understanding the regulatory role of clock proteins in circadian rhythms, how chromatin organization affects circadian rhythms remains poorly understood. Here, we employed ATAC-seq (Assay for Transposase-Accessible Chromatin with Sequencing) on FAC-sorted Drosophila clock neurons to assess genome-wide chromatin accessibility at dawn and dusk over the circadian cycle. We observed significant oscillations in chromatin accessibility at promoter and enhancer regions of hundreds of genes, with enhanced accessibility either at dusk or dawn, which correlated with their peak transcriptional activity. Notably, genes with enhanced accessibility at dusk were enriched with E-box motifs, while those more accessible at dawn were enriched with VRI/PDP1-box motifs, indicating that they are regulated by the core circadian feedback loops, PER/CLK and VRI/PDP1, respectively. Further, we observed a complete loss of chromatin accessibility rhythms in </span><em>per</em><sup><em>01</em></sup><span><span> </span>null mutants, with chromatin consistently accessible at both dawn and dusk, underscoring the critical role of Period protein in driving chromatin compaction during the repression phase at dawn. Together, this study demonstrates the significant role of chromatin organization in circadian regulation, revealing how the interplay between clock proteins and chromatin structure orchestrates the precise timing of biological processes throughout the day. This work further implies that variations in chromatin accessibility might play a central role in the generation of diverse circadian gene expression patterns in clock neurons.</span></p>',
'date' => '2024-05-28',
'pmid' => 'https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1011278',
'doi' => 'https://doi.org/10.1371/journal.pgen.1011278',
'modified' => '2025-02-26 17:21:25',
'created' => '2025-02-26 17:21:25',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 9 => array(
'id' => '5062',
'name' => 'PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites',
'authors' => 'Andrew Dimond et al.',
'description' => '<p><span>PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in </span><em>Pbk<sup>−/−</sup></em><span>preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by<span> </span></span><em>Ikzf1</em><span>,<span> </span></span><em>Ikzf3</em><span>,<span> </span></span><em>Znf131</em><span><span> </span>and<span> </span></span><em>Zbtb11</em><span>. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction.</span></p>',
'date' => '2024-04-23',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.23.590758v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.04.23.590758',
'modified' => '2025-02-26 17:22:58',
'created' => '2025-02-26 17:22:58',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 10 => array(
'id' => '5057',
'name' => 'Widespread impact of nucleosome remodelers on transcription at cis-regulatory elements',
'authors' => 'Benjamin J. Patty et al.',
'description' => '<p><span>Nucleosome remodeling complexes and other regulatory factors work in concert to build a chromatin environment that directs the expression of a distinct set of genes in each cell using cis-regulatory elements (CREs), such as promoters and enhancers, that drive transcription of both mRNAs and CRE-associated non-coding RNAs (ncRNAs). Two classes of CRE-associated ncRNAs include upstream antisense RNAs (uaRNAs), which are transcribed divergently from a shared mRNA promoter, and enhancer RNAs (eRNAs), which are transcribed bidirectionally from active enhancers. The complicated network of CRE regulation by nucleosome remodelers remains only partially explored, with a focus on a select, limited number of remodelers. We endeavored to elucidate a remodeler-based regulatory network governing CRE-associated transcription (mRNA, eRNA, and uaRNA) in murine embryonic stem (ES) cells to test the hypothesis that many SNF2-family nucleosome remodelers collaborate to regulate the coding and non-coding transcriptome via alteration of underlying nucleosome architecture. Using depletion followed by transient transcriptome sequencing (TT-seq), we identified thousands of misregulated mRNAs and CRE-associated ncRNAs across the remodelers examined, identifying novel contributions by understudied remodelers in the regulation of coding and non-coding transcription. Our findings suggest that mRNA and eRNA transcription are coordinately co-regulated, while mRNA and uaRNAs sharing a common promoter are independently regulated. Subsequent mechanistic studies suggest that while remodelers SRCAP and CHD8 modulate transcription through classical mechanisms such as transcription factors and histone variants, a broad set of remodelers including SMARCAL1 indirectly contribute to transcriptional regulation through maintenance of genomic stability and proper Integrator complex localization. This study systematically examines the contribution of SNF2-remodelers to the CRE-associated transcriptome, identifying at least two classes for remodeler action.</span></p>',
'date' => '2024-04-15',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.12.589208v1',
'doi' => 'https://doi.org/10.1101/2024.04.12.589208',
'modified' => '2025-02-26 17:09:18',
'created' => '2025-02-26 17:09:18',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 11 => array(
'id' => '4926',
'name' => 'High-throughput sequencing of insect specimens with sub-optimal DNA preservation using a practical, plate-based Illumina-compatible Tn5 transposase library preparation method',
'authors' => 'Cobb L. et all.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we use a practical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs that were stored under sub-optimal conditions for DNA preservation. The samples were kept in field vehicles for extended periods of time, before long-term storage in ethanol in the freezer, or dry at room temperature. By reducing DNA input to 6ng, more samples with sub-optimal DNA yields could be processed. We matched this low DNA input with a 6-fold dilution of a commercially available tagmentation enzyme, significantly reducing library preparation costs. Costs and workload were further suppressed by direct post-amplification pooling of individual libraries. We generated medium coverage (>3-fold) genomes for 88 out of 90 specimens, with an average of approximately 10-fold coverage. While samples stored in ethanol yielded significantly less DNA compared to those which were stored dry, these samples had superior sequencing statistics, with longer sequencing reads and higher rates of endogenous DNA. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by a thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By opening opportunities for the use of sub-optimally preserved, low yield DNA extracts, we broaden the scope of whole genome studies of insect specimens. We therefore expect these results and this protocol to be valuable for a range of applications in the field of entomology.</span></p>',
'date' => '2024-03-22',
'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/38517905/',
'doi' => '10.1371/journal.pone.0300865',
'modified' => '2024-03-25 11:15:06',
'created' => '2024-03-25 11:15:06',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 12 => array(
'id' => '4923',
'name' => 'On the identification of differentially-active transcription factors from ATAC-seq data',
'authors' => 'Gerbaldo F. et al.',
'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (chromVAR-limma with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs – in our case NFkB – at the protein level.</span></p>',
'date' => '2024-03-10',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.03.06.583825v2',
'doi' => 'https://doi.org/10.1101/2024.03.06.583825',
'modified' => '2024-03-13 17:04:33',
'created' => '2024-03-13 17:04:33',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 13 => array(
'id' => '5003',
'name' => 'Improved metagenome assemblies through selective enrichment of bacterial genomic DNA from eukaryotic host genomic DNA using ATAC-seq',
'authors' => 'Lindsey J Cantin et al.',
'description' => '<p><span>Genomics can be used to study the complex relationships between hosts and their microbiota. Many bacteria cannot be cultured in the laboratory, making it difficult to obtain adequate amounts of bacterial DNA and to limit host DNA contamination for the construction of metagenome-assembled genomes (MAGs). For example, </span><em>Wolbachia</em><span><span> </span>is a genus of exclusively obligate intracellular bacteria that live in a wide range of arthropods and some nematodes. While<span> </span></span><em>Wolbachia</em><span><span> </span>endosymbionts are frequently described as facultative reproductive parasites in arthropods, the bacteria are obligate mutualistic endosymbionts of filarial worms. Here, we achieve 50-fold enrichment of bacterial sequences using ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) with<span> </span></span><em>Brugia malayi</em><span><span> </span>nematodes, containing<span> </span></span><em>Wolbachia</em><span><span> </span>(</span><em>w</em><span>Bm). ATAC-seq uses the Tn5 transposase to cut and attach Illumina sequencing adapters to accessible DNA lacking histones, typically thought to be open chromatin. Bacterial and mitochondrial DNA in the lysates are also cut preferentially since they lack histones, leading to the enrichment of these sequences. The benefits of this include minimal tissue input (<1 mg of tissue), a quick protocol (<4 h), low sequencing costs, less bias, correct assembly of lateral gene transfers and no prior sequence knowledge required. We assembled the<span> </span></span><em>w</em><span>Bm genome with as few as 1 million Illumina short paired-end reads with >97% coverage of the published genome, compared to only 12% coverage with the standard gDNA libraries. We found significant bacterial sequence enrichment that facilitated genome assembly in previously published ATAC-seq data sets from human cells infected with<span> </span></span><em>Mycobacterium tuberculosis</em><span><span> </span>and<span> </span></span><em>C. elegans</em><span><span> </span>contaminated with their food source, the OP50 strain of<span> </span></span><em>E. coli</em><span>. These results demonstrate the feasibility and benefits of using ATAC-seq to easily obtain bacterial genomes to aid in symbiosis, infectious disease, and microbiome research.</span></p>',
'date' => '2024-02-15',
'pmid' => 'https://pmc.ncbi.nlm.nih.gov/articles/PMC10902005/',
'doi' => '10.3389/fmicb.2024.1352378',
'modified' => '2024-11-29 11:10:24',
'created' => '2024-11-29 11:10:24',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 14 => array(
'id' => '5063',
'name' => 'A fast and inexpensive plate-based NGS library preparation method for insect genomics',
'authors' => 'Lauren Cobb et al.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we investigate a fast and economical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs stored under different conditions. Using a standardised input of 6ng DNA, library preparation costs were significantly reduced through the 6-fold dilution of a commercially available tagmentation enzyme. Costs were further suppressed by direct post-amplification pooling, skipping quality assessment of individual libraries. We find that reduced DNA yields associated with ethanol-based storage do not impede overall sequencing success. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By lowering data generation costs, broadening the scope of whole genome studies to include low yield DNA extracts and increasing throughput, we expect this protocol to be of significant value for a range of applications in the field of insect genomics.</span></p>',
'date' => '2023-11-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.11.24.568434v1.abstract',
'doi' => 'https://doi.org/10.1101/2023.11.24.568434',
'modified' => '2025-02-26 17:24:46',
'created' => '2025-02-26 17:24:46',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 15 => array(
'id' => '5060',
'name' => 'Therapeutic targeting of EP300/CBP by bromodomain inhibition in hematologic malignancies',
'authors' => 'Luciano Nicosia et al. ',
'description' => '<p><span>CCS1477 (inobrodib) is a potent, selective EP300/CBP bromodomain inhibitor which induces cell-cycle arrest and differentiation in hematologic malignancy model systems. In myeloid leukemia cells, it promotes rapid eviction of EP300/CBP from an enhancer subset marked by strong MYB occupancy and high H3K27 acetylation, with downregulation of the subordinate oncogenic network and redistribution to sites close to differentiation genes. In myeloma cells, CCS1477 induces eviction of EP300/CBP from </span><i>FGFR3</i><span>, the target of the common (4; 14) translocation, with redistribution away from IRF4-occupied sites to TCF3/E2A-occupied sites. In a subset of patients with relapsed or refractory disease, CCS1477 monotherapy induces differentiation responses in AML and objective responses in heavily pre-treated multiple myeloma.<span> </span></span><i>In vivo</i><span><span> </span>preclinical combination studies reveal synergistic responses to treatment with standard-of-care agents. Thus, CCS1477 exhibits encouraging preclinical and early-phase clinical activity by disrupting recruitment of EP300/CBP to enhancer networks occupied by critical transcription factors.</span></p>',
'date' => '2023-11-22',
'pmid' => 'https://www.cell.com/cancer-cell/fulltext/S1535-6108(23)00366-5',
'doi' => '10.1016/j.ccell.2023.11.001',
'modified' => '2025-02-26 17:15:25',
'created' => '2025-02-26 17:15:25',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 16 => array(
'id' => '4878',
'name' => 'ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse',
'authors' => 'Menon D.U. et al.',
'description' => '<p><span>We present evidence implicating the BAF (BRG1/BRM Associated Factor) chromatin remodeler in meiotic sex chromosome inactivation (MSCI). By immunofluorescence (IF), the putative BAF DNA binding subunit, ARID1A (AT-rich Interaction Domain 1a), appeared enriched on the male sex chromosomes during diplonema of meiosis I. The germ cell-specific depletion of ARID1A resulted in a pachynema arrest and failure to repress sex-linked genes, indicating a defective MSCI. Consistent with this defect, mutant sex chromosomes displayed an abnormal presence of elongating RNA polymerase II coupled with an overall increase in chromatin accessibility detectable by ATAC-seq. By investigating potential mechanisms underlying these anomalies, we identified a role for ARID1A in promoting the preferential enrichment of the histone variant, H3.3, on the sex chromosomes, a known hallmark of MSCI. Without ARID1A, the sex chromosomes appeared depleted of H3.3 at levels resembling autosomes. Higher resolution analyses by CUT&RUN revealed shifts in sex-linked H3.3 associations from discrete intergenic sites and broader gene-body domains to promoters in response to the loss of ARID1A. Several sex-linked sites displayed ectopic H3.3 occupancy that did not co-localize with DMC1 (DNA Meiotic Recombinase 1). This observation suggests a requirement for ARID1A in DMC1 localization to the asynapsed sex chromatids. We conclude that ARID1A-directed H3.3 localization influences meiotic sex chromosome gene regulation and DNA repair.</span></p>',
'date' => '2023-09-28',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.25.542290v2.abstract',
'doi' => 'https://doi.org/10.1101/2023.05.25.542290',
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'name' => 'CXCR4 signaling strength regulates hematopoietic multipotent progenitor fate through extrinsic and intrinsic mechanisms',
'authors' => 'Vincent Rondeau et al.',
'description' => '<p><span>How cell-extrinsic niche-related and cell-intrinsic cues drive lineage specification of hematopoietic multipotent progenitors (MPPs) in the bone marrow (BM) is partly understood. We show that CXCR4 signaling strength regulates localization and fate of MPPs. In mice phenocopying the BM myeloid skewing of patients with WHIM Syndrome (WS), a rare immunodeficiency caused by gain-of-function </span><em>CXCR4</em><span><span> </span>mutations, enhanced mTOR signaling and overactive Oxphos metabolism were associated with myeloid rewiring of lymphoid-primed MPPs (or MPP4). Fate decision of MPP4 was also affected by molecular changes established at the MPP1 level. Mutant MPP4 displayed altered BM localization relative to peri-arteriolar structures, suggesting that extrinsic cues contribute to their myeloid skewing. Chronic treatment with CXCR4 antagonist AMD3100 or mTOR inhibitor Rapamycin rescued lymphoid capacities of mutant MPP4, demonstrating a pivotal role for the CXCR4-mTOR axis in regulating MPP4 fate. Our study thus provides mechanistic insights into how CXCR4 signaling regulates the lymphoid potential of MPPs.</span></p>',
'date' => '2023-06-01',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.31.542899v1.abstract',
'doi' => 'https://doi.org/10.1101/2023.05.31.542899',
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'description' => '<p><span>Tumor-initiating cells are major drivers of chemoresistance and attractive targets for cancer therapy, however, their identity in human pancreatic ductal adenocarcinoma (PDAC) and the key molecules underlying their traits remain poorly understood. Here, we show that a cellular subpopulation with partial epithelial-mesenchymal transition (EMT)-like signature marked by high expression of receptor tyrosine kinase-like orphan receptor 1 (ROR1) is the origin of heterogeneous tumor cells in PDAC. We demonstrate that ROR1 depletion suppresses tumor growth, recurrence after chemotherapy, and metastasis. Mechanistically, ROR1 induces the expression of Aurora kinase B (AURKB) by activating E2F through c-Myc to enhance PDAC proliferation. Furthermore, epigenomic analyses reveal that ROR1 is transcriptionally dependent on YAP/BRD4 binding at the enhancer region, and targeting this pathway reduces ROR1 expression and prevents PDAC growth. Collectively, our findings reveal a critical role for ROR1high cells as tumor-initiating cells and the functional importance of ROR1 in PDAC progression, thereby highlighting its therapeutic targetability.</span></p>',
'date' => '2023-04-01',
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'name' => 'A neurodevelopmental epigenetic programme mediated bySMARCD3-DAB1-Reelin signalling is hijacked to promote medulloblastomametastasis.',
'authors' => 'Zou Han et al.',
'description' => '<p>How abnormal neurodevelopment relates to the tumour aggressiveness of medulloblastoma (MB), the most common type of embryonal tumour, remains elusive. Here we uncover a neurodevelopmental epigenomic programme that is hijacked to induce MB metastatic dissemination. Unsupervised analyses of integrated publicly available datasets with our newly generated data reveal that SMARCD3 (also known as BAF60C) regulates Disabled 1 (DAB1)-mediated Reelin signalling in Purkinje cell migration and MB metastasis by orchestrating cis-regulatory elements at the DAB1 locus. We further identify that a core set of transcription factors, enhancer of zeste homologue 2 (EZH2) and nuclear factor I X (NFIX), coordinates with the cis-regulatory elements at the SMARCD3 locus to form a chromatin hub to control SMARCD3 expression in the developing cerebellum and in metastatic MB. Increased SMARCD3 expression activates Reelin-DAB1-mediated Src kinase signalling, which results in a MB response to Src inhibition. These data deepen our understanding of how neurodevelopmental programming influences disease progression and provide a potential therapeutic option for patients with MB.</p>',
'date' => '2023-02-01',
'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36849558',
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'modified' => '2023-03-14 09:41:24',
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'description' => '<p>The establishment of de novo chromatin accessibility in lymphoid progenitors requires the "pioneering" function of transcription factor (TF) early B cell factor 1 (EBF1), which binds to naïve chromatin and induces accessibility by recruiting the BRG1 chromatin remodeler subunit. However, it remains unclear whether the function of EBF1 is continuously required for stabilizing local chromatin accessibility. To this end, we replaced EBF1 by EBF1-FKBP in pro-B cells, allowing the rapid degradation by adding the degradation TAG13 (dTAG13) dimerizer. EBF1 degradation results in a loss of genome-wide EBF1 occupancy and EBF1-targeted BRG1 binding. Chromatin accessibility was rapidly diminished at EBF1-binding sites with a preference for sites whose occupancy requires the pioneering activity of the C-terminal domain of EBF1. Diminished chromatin accessibility correlated with altered gene expression. Thus, continuous activity of EBF1 is required for the stable maintenance of the transcriptional and epigenetic state of pro-B cells.</p>',
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<td style="width: 326px;">Tagmentation Buffer (2x)</td>
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<li>After cell lysis and nuclei isolation, the nuclei pellets can be incubated with the following mix for 1 reaction:</li>
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<td style="width: 326px;">Tagmentation Buffer (2x)</td>
<td style="width: 114px; padding-left: 30px;">25 µl</td>
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<li>The reaction is then incubated 30 minutes at 37°C.</li>
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<p>Diagenode <strong>Tagmentation Buffer (2x)</strong> is the recommended reagent to perform any tagmentation reactions. It can be used in combination with Diagenode <a href="https://www.diagenode.com/en/p/tagmentase-loaded-30">Tagmentase (Tn5 transposase)</a> on DNA or chromatin samples, as half of the total volume reaction like in ATAC-seq protocol.</p>
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<ul style="list-style-type: circle;">
<li>After cell lysis and nuclei isolation, the nuclei pellets can be incubated with the following mix for 1 reaction:</li>
</ul>
<table style="width: 447px;">
<tbody>
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<td style="width: 326px;">Tagmentation Buffer (2x)</td>
<td style="width: 114px; padding-left: 30px;">25 µl</td>
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<li>The reaction is then incubated 30 minutes at 37°C.</li>
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<li>The tagmented libraries can then be purified using the MicroChIP DiaPure Columns (Cat. No. C03040001), and amplified.</li>
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'name' => 'Combinatorial mapping of E3 ubiquitin ligases to their target substrates',
'authors' => 'Chase C. Suiter et al.',
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<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">Developed a combinatorial assay to test E3-substrate interactions at scale</div>
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<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">Identified known and unknown E3-substrate relationships across three screens</div>
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<div class="content">
<div id="p0020" role="paragraph">Assessment of<span> </span><i>in silico</i><span> </span>models points to scalable computational substrate discovery</div>
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<div class="content">
<div id="p0025" role="paragraph">Computed models of E3-substrate interactions reveal known and putative degron motifs</div>
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<div id="abspara0010" role="paragraph">E3 ubiquitin ligases (E3s) confer specificity of protein degradation through ubiquitination of substrate proteins. Yet, the vast majority of the >600 human E3s have no known substrates. To identify proteolytic E3-substrate pairs at scale, we developed combinatorial mapping of E3 targets (COMET), a framework for testing the role of many E3s in degrading many candidate substrates within a single experiment. We applied COMET to SCF ubiquitin ligase subunits that mediate degradation of target substrates (6,716 F-box-ORF [open reading frame] combinations) and E3s that degrade short-lived transcription factors (TFs) (26,028 E3-TF combinations). Our data suggest that many E3-substrate relationships are complex rather than 1:1 associations. Finally, we leverage deep learning to predict the structural basis of E3-substrate interactions and probe the strengths and limits of such models. Looking forward, we consider the practicality of transposing this framework, i.e., computational structural prediction of all possible E3-substrate interactions, followed by multiplex experimental validation.</div>
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'pmid' => 'https://www.cell.com/molecular-cell/fulltext/S1097-2765(25)00051-6',
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'name' => 'Minimization of gene editing off-target effects by tissue restriction of expression',
'authors' => 'Nam-Gyun Kim et al.',
'description' => '<p><span>Therapeutic </span><em>in vivo</em><span><span> </span>gene editing with highly specific nucleases has the potential to revolutionize treatment for a wide range of human diseases, including genetic disorders and latent viral infections like herpes simplex virus (HSV). However, challenges regarding specificity, efficiency, delivery, and safety must be addressed before its clinical application. A key concern is the risk of off-target effects, which can cause unintended and potentially harmful genetic changes. We previously developed a curative<span> </span></span><em>in vivo</em><span><span> </span>gene editing approach to eliminate latent HSV using HSV-specific meganuclease delivered by an AAV vector. In this study, we investigate off-target effects of meganuclease by identifying potential off-target sites through GUIDE-tag analysis and assessing genetic alterations using amplicon deep sequencing in tissues from meganuclease treated mice. Our results show that meganuclease expression driven by a ubiquitous promoter leads to high off-target gene editing in the mouse liver, a non-relevant target tissue. However, restricting the meganuclease expression with a neuron-specific promoter and/or a liver-specific miRNA target sequence efficiently reduces off-target effects in both liver and trigeminal ganglia. These findings suggest that incorporation of regulatory DNA elements for tissue-specific expression in viral vectors can reduce off-target effects and improve the safety of therapeutic<span> </span></span><em>in vivo</em><span><span> </span>gene editing.</span></p>',
'date' => '2025-01-21',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2025.01.21.634017v1',
'doi' => 'https://doi.org/10.1101/2025.01.21.634017',
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'name' => 'HIRA protects telomeres against R-loop-induced instability in ALT cancer cells',
'authors' => 'Michelle Lee Lynskey et al.',
'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HIRA establishes greater telomeric chromatin accessibility after ATRX-DAXX loss</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">Deposition of new H3.3 by HIRA-UBN restricts telomeric ssDNA and TERRA R-loops</div>
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</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">Unresolved TERRA R-loops block new H3.3 deposition by HIRA-UBN</div>
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</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">CHK1 phosphorylation of H3.3 is critical to prevent ssDNA and TERRA R-loop buildup</div>
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</div>
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<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">Inactivating mutations in chromatin modifiers, like the α-thalassemia/mental retardation, X-linked (ATRX)-death domain-associated protein (DAXX) chromatin remodeling/histone H3.3 deposition complex, drive the cancer-specific alternative lengthening of telomeres (ALT) pathway. Prior studies revealed that HIRA, another histone H3.3 chaperone, compensates for ATRX-DAXX loss at telomeres to sustain ALT cancer cell survival. How HIRA rescues telomeres from the consequences of ATRX-DAXX deficiency remains unclear. Here, using an assay for transposase-accessible chromatin using sequencing (ATAC-seq) and cleavage under targets and release using nuclease (CUT&RUN), we establish that HIRA-mediated deposition of new H3.3 maintains telomeric chromatin accessibility to prevent the detrimental accumulation of nucleosome-free single-stranded DNA (ssDNA) in ATRX-DAXX-deficient ALT cells. We show that the HIRA-UBN1/UBN2 complex deposits new H3.3 to prevent TERRA R-loop buildup and transcription-replication conflicts (TRCs) at telomeres. Furthermore, HIRA-mediated H3.3 incorporation into telomeric chromatin links productive ALT to the phosphorylation of serine 31, an H3.3-specific amino acid, by Chk1. Therefore, we identify a critical role for HIRA-mediated H3.3 deposition that ensures the survival of ATRX-DAXX-deficient ALT cancer cells.</div>
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'date' => '2024-11-26',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01315-9',
'doi' => '10.1016/j.celrep.2024.114964',
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'name' => 'Enhancing single-cell ATAC sequencing with formaldehyde fixation, cryopreservation, and multiplexing for flexible analysis',
'authors' => 'Tobias Hohl et al.',
'description' => '<p><span>The assay for transposase-accessible chromatin using sequencing (ATAC-seq) revolutionized the field of epigenetics since its emergence by providing a means to uncover chromatin dynamics and other factors affecting gene expression. The development of single-cell (sc) applications in recent years led to an even deeper understanding of cell type specific gene regulatory mechanisms. One of the major challenges while running ATAC-seq experiments, bulk or sc, is the need for freshly collected cells for successful experiments. While various freezing methods have already been tested and established for bulk and sc ATAC-seq, quality metrics for preserved cells are rather poor or dependent on sampling time when compared to fresh samples. This makes it difficult to conduct all sorts of complex experiments i.e. with multiple conditions, patients, or time course studies. Especially, accounting for batch effects can be difficult if samples need to be processed at different time points of collection. We tackled this issue by adding a fixation step prior to the freezing method. The additional fixation step improved library quality and yield data comparable to fresh samples. The workflow was also tested on multiplexed sc ATAC experiments, set-up for cost-efficient low input sample handling. Sample cross-in, typically encountered in Tn5-based multiplex approaches, were tackled with a computational procedure specifically developed for this approach.</span></p>',
'date' => '2024-11-21',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.11.20.624480v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.11.20.624480',
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'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (a chromVAR-limma workflow with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs—in our case NFkB—at the protein level.</span></p>',
'date' => '2024-10-23',
'pmid' => 'https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1011971',
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'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
'authors' => 'Alessia Bagattin et al.',
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<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
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<div id="p0010" role="paragraph">HNF1β mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
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<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1β partner, mediates mitosis-specific interaction with TOP1</div>
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<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1β recruits TOP1 and induces DNA relaxation around bookmarked HNF1β sites</div>
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<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1β mutation, found in MODY patients, disrupts the interaction with TOP1</div>
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<div id="abspara0010" role="paragraph">HNF1β (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that HNF1β remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1β-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1β and TOP1, where a mutation, found in “maturity onset diabetes of the young” patients, disrupts their interaction. Importantly, HNF1β recruits TOP1 and induces DNA relaxation around HNF1β mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1β reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
'date' => '2024-10-08',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
'doi' => '10.1016/j.celrep.2024.114805',
'modified' => '2024-10-14 09:04:44',
'created' => '2024-10-14 09:04:44',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 6 => array(
'id' => '5056',
'name' => 'Rhabdomyosarcoma fusion oncoprotein initially pioneers a neural signature in vivo',
'authors' => 'Jack Kucinski et al.',
'description' => '<p><span>Fusion-positive rhabdomyosarcoma is an aggressive pediatric cancer molecularly characterized by arrested myogenesis. The defining genetic driver, PAX3::FOXO1, functions as a chimeric gain-of-function transcription factor. An incomplete understanding of PAX3::FOXO1’s in vivo epigenetic mechanisms has hindered therapeutic development. Here, we establish a PAX3::FOXO1 zebrafish injection model and semi-automated ChIP-seq normalization strategy to evaluate how PAX3::FOXO1 initially interfaces with chromatin in a developmental context. We investigated PAX3::FOXO1’s recognition of chromatin and subsequent transcriptional consequences. We find that PAX3::FOXO1 interacts with inaccessible chromatin through partial/homeobox motif recognition consistent with pioneering activity. However, PAX3::FOXO1-genome binding through a composite paired-box/homeobox motif alters chromatin accessibility and redistributes H3K27ac to activate neural transcriptional programs. We uncover neural signatures that are highly representative of clinical rhabdomyosarcoma gene expression programs that are enriched following chemotherapy. Overall, we identify partial/homeobox motif recognition as a new mode for PAX3::FOXO1 pioneer function and identify neural signatures as a potentially critical PAX3::FOXO1 tumor initiation event.</span></p>',
'date' => '2024-07-16',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.07.12.603270v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.07.12.603270',
'modified' => '2025-02-26 17:07:24',
'created' => '2025-02-26 17:07:24',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 7 => array(
'id' => '5058',
'name' => 'CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly',
'authors' => 'Hanna Schwaemmle et al.',
'description' => '<p><span>The SWI/SNF (or BAF) complex is an essential chromatin remodeler that regulates DNA accessibility at developmental genes and enhancers. SWI/SNF subunits are among the most frequently mutated genes in cancer and neurodevelopmental disorders. These mutations are often heterozygous loss-of-function alleles, indicating a dosage-sensitive role for SWI/SNF subunits in chromatin regulation. However, the molecular mechanisms that regulate SWI/SNF subunit dosage to ensure proper complex assembly remain largely unexplored. We performed a genome-wide CRISPR KO screen, using epigenome editing in mouse embryonic stem cells, and identified </span><em>Mlf2</em><span><span> </span>and<span> </span></span><em>Rbm15</em><span><span> </span>as regulators of SWI/SNF complex activity. First, we show that MLF2, a poorly characterized chaperone protein, regulates a subset of SWI/SNF target genes by promoting chromatin remodeling activity. Next, we find that RBM15, part of the m</span><sup>6</sup><span>A RNA methylation writer complex, controls m</span><sup>6</sup><span>A modifications on specific SWI/SNF mRNAs to regulate protein levels of these subunits. Misregulation of m</span><sup>6</sup><span>A methylation causes overexpression of core SWI/SNF subunits leading to the assembly of incomplete complexes lacking the catalytic ATPase/ARP subunits. These data indicate that targeting modulators of SWI/SNF complex assembly may offer a potent therapeutic strategy for diseases associated with impaired chromatin remodeling.</span></p>',
'date' => '2024-06-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.06.25.600572v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.06.25.600572',
'modified' => '2025-02-26 17:10:53',
'created' => '2025-02-26 17:10:53',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 8 => array(
'id' => '5061',
'name' => 'Clock-dependent chromatin accessibility rhythms regulate circadian transcription',
'authors' => 'Ye Yuan et al.',
'description' => '<p><span>Chromatin organization plays a crucial role in gene regulation by controlling the accessibility of DNA to transcription machinery. While significant progress has been made in understanding the regulatory role of clock proteins in circadian rhythms, how chromatin organization affects circadian rhythms remains poorly understood. Here, we employed ATAC-seq (Assay for Transposase-Accessible Chromatin with Sequencing) on FAC-sorted Drosophila clock neurons to assess genome-wide chromatin accessibility at dawn and dusk over the circadian cycle. We observed significant oscillations in chromatin accessibility at promoter and enhancer regions of hundreds of genes, with enhanced accessibility either at dusk or dawn, which correlated with their peak transcriptional activity. Notably, genes with enhanced accessibility at dusk were enriched with E-box motifs, while those more accessible at dawn were enriched with VRI/PDP1-box motifs, indicating that they are regulated by the core circadian feedback loops, PER/CLK and VRI/PDP1, respectively. Further, we observed a complete loss of chromatin accessibility rhythms in </span><em>per</em><sup><em>01</em></sup><span><span> </span>null mutants, with chromatin consistently accessible at both dawn and dusk, underscoring the critical role of Period protein in driving chromatin compaction during the repression phase at dawn. Together, this study demonstrates the significant role of chromatin organization in circadian regulation, revealing how the interplay between clock proteins and chromatin structure orchestrates the precise timing of biological processes throughout the day. This work further implies that variations in chromatin accessibility might play a central role in the generation of diverse circadian gene expression patterns in clock neurons.</span></p>',
'date' => '2024-05-28',
'pmid' => 'https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1011278',
'doi' => 'https://doi.org/10.1371/journal.pgen.1011278',
'modified' => '2025-02-26 17:21:25',
'created' => '2025-02-26 17:21:25',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 9 => array(
'id' => '5062',
'name' => 'PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites',
'authors' => 'Andrew Dimond et al.',
'description' => '<p><span>PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in </span><em>Pbk<sup>−/−</sup></em><span>preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by<span> </span></span><em>Ikzf1</em><span>,<span> </span></span><em>Ikzf3</em><span>,<span> </span></span><em>Znf131</em><span><span> </span>and<span> </span></span><em>Zbtb11</em><span>. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction.</span></p>',
'date' => '2024-04-23',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.23.590758v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.04.23.590758',
'modified' => '2025-02-26 17:22:58',
'created' => '2025-02-26 17:22:58',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 10 => array(
'id' => '5057',
'name' => 'Widespread impact of nucleosome remodelers on transcription at cis-regulatory elements',
'authors' => 'Benjamin J. Patty et al.',
'description' => '<p><span>Nucleosome remodeling complexes and other regulatory factors work in concert to build a chromatin environment that directs the expression of a distinct set of genes in each cell using cis-regulatory elements (CREs), such as promoters and enhancers, that drive transcription of both mRNAs and CRE-associated non-coding RNAs (ncRNAs). Two classes of CRE-associated ncRNAs include upstream antisense RNAs (uaRNAs), which are transcribed divergently from a shared mRNA promoter, and enhancer RNAs (eRNAs), which are transcribed bidirectionally from active enhancers. The complicated network of CRE regulation by nucleosome remodelers remains only partially explored, with a focus on a select, limited number of remodelers. We endeavored to elucidate a remodeler-based regulatory network governing CRE-associated transcription (mRNA, eRNA, and uaRNA) in murine embryonic stem (ES) cells to test the hypothesis that many SNF2-family nucleosome remodelers collaborate to regulate the coding and non-coding transcriptome via alteration of underlying nucleosome architecture. Using depletion followed by transient transcriptome sequencing (TT-seq), we identified thousands of misregulated mRNAs and CRE-associated ncRNAs across the remodelers examined, identifying novel contributions by understudied remodelers in the regulation of coding and non-coding transcription. Our findings suggest that mRNA and eRNA transcription are coordinately co-regulated, while mRNA and uaRNAs sharing a common promoter are independently regulated. Subsequent mechanistic studies suggest that while remodelers SRCAP and CHD8 modulate transcription through classical mechanisms such as transcription factors and histone variants, a broad set of remodelers including SMARCAL1 indirectly contribute to transcriptional regulation through maintenance of genomic stability and proper Integrator complex localization. This study systematically examines the contribution of SNF2-remodelers to the CRE-associated transcriptome, identifying at least two classes for remodeler action.</span></p>',
'date' => '2024-04-15',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.12.589208v1',
'doi' => 'https://doi.org/10.1101/2024.04.12.589208',
'modified' => '2025-02-26 17:09:18',
'created' => '2025-02-26 17:09:18',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 11 => array(
'id' => '4926',
'name' => 'High-throughput sequencing of insect specimens with sub-optimal DNA preservation using a practical, plate-based Illumina-compatible Tn5 transposase library preparation method',
'authors' => 'Cobb L. et all.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we use a practical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs that were stored under sub-optimal conditions for DNA preservation. The samples were kept in field vehicles for extended periods of time, before long-term storage in ethanol in the freezer, or dry at room temperature. By reducing DNA input to 6ng, more samples with sub-optimal DNA yields could be processed. We matched this low DNA input with a 6-fold dilution of a commercially available tagmentation enzyme, significantly reducing library preparation costs. Costs and workload were further suppressed by direct post-amplification pooling of individual libraries. We generated medium coverage (>3-fold) genomes for 88 out of 90 specimens, with an average of approximately 10-fold coverage. While samples stored in ethanol yielded significantly less DNA compared to those which were stored dry, these samples had superior sequencing statistics, with longer sequencing reads and higher rates of endogenous DNA. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by a thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By opening opportunities for the use of sub-optimally preserved, low yield DNA extracts, we broaden the scope of whole genome studies of insect specimens. We therefore expect these results and this protocol to be valuable for a range of applications in the field of entomology.</span></p>',
'date' => '2024-03-22',
'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/38517905/',
'doi' => '10.1371/journal.pone.0300865',
'modified' => '2024-03-25 11:15:06',
'created' => '2024-03-25 11:15:06',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 12 => array(
'id' => '4923',
'name' => 'On the identification of differentially-active transcription factors from ATAC-seq data',
'authors' => 'Gerbaldo F. et al.',
'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (chromVAR-limma with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs – in our case NFkB – at the protein level.</span></p>',
'date' => '2024-03-10',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.03.06.583825v2',
'doi' => 'https://doi.org/10.1101/2024.03.06.583825',
'modified' => '2024-03-13 17:04:33',
'created' => '2024-03-13 17:04:33',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 13 => array(
'id' => '5003',
'name' => 'Improved metagenome assemblies through selective enrichment of bacterial genomic DNA from eukaryotic host genomic DNA using ATAC-seq',
'authors' => 'Lindsey J Cantin et al.',
'description' => '<p><span>Genomics can be used to study the complex relationships between hosts and their microbiota. Many bacteria cannot be cultured in the laboratory, making it difficult to obtain adequate amounts of bacterial DNA and to limit host DNA contamination for the construction of metagenome-assembled genomes (MAGs). For example, </span><em>Wolbachia</em><span><span> </span>is a genus of exclusively obligate intracellular bacteria that live in a wide range of arthropods and some nematodes. While<span> </span></span><em>Wolbachia</em><span><span> </span>endosymbionts are frequently described as facultative reproductive parasites in arthropods, the bacteria are obligate mutualistic endosymbionts of filarial worms. Here, we achieve 50-fold enrichment of bacterial sequences using ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) with<span> </span></span><em>Brugia malayi</em><span><span> </span>nematodes, containing<span> </span></span><em>Wolbachia</em><span><span> </span>(</span><em>w</em><span>Bm). ATAC-seq uses the Tn5 transposase to cut and attach Illumina sequencing adapters to accessible DNA lacking histones, typically thought to be open chromatin. Bacterial and mitochondrial DNA in the lysates are also cut preferentially since they lack histones, leading to the enrichment of these sequences. The benefits of this include minimal tissue input (<1 mg of tissue), a quick protocol (<4 h), low sequencing costs, less bias, correct assembly of lateral gene transfers and no prior sequence knowledge required. We assembled the<span> </span></span><em>w</em><span>Bm genome with as few as 1 million Illumina short paired-end reads with >97% coverage of the published genome, compared to only 12% coverage with the standard gDNA libraries. We found significant bacterial sequence enrichment that facilitated genome assembly in previously published ATAC-seq data sets from human cells infected with<span> </span></span><em>Mycobacterium tuberculosis</em><span><span> </span>and<span> </span></span><em>C. elegans</em><span><span> </span>contaminated with their food source, the OP50 strain of<span> </span></span><em>E. coli</em><span>. These results demonstrate the feasibility and benefits of using ATAC-seq to easily obtain bacterial genomes to aid in symbiosis, infectious disease, and microbiome research.</span></p>',
'date' => '2024-02-15',
'pmid' => 'https://pmc.ncbi.nlm.nih.gov/articles/PMC10902005/',
'doi' => '10.3389/fmicb.2024.1352378',
'modified' => '2024-11-29 11:10:24',
'created' => '2024-11-29 11:10:24',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 14 => array(
'id' => '5063',
'name' => 'A fast and inexpensive plate-based NGS library preparation method for insect genomics',
'authors' => 'Lauren Cobb et al.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we investigate a fast and economical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs stored under different conditions. Using a standardised input of 6ng DNA, library preparation costs were significantly reduced through the 6-fold dilution of a commercially available tagmentation enzyme. Costs were further suppressed by direct post-amplification pooling, skipping quality assessment of individual libraries. We find that reduced DNA yields associated with ethanol-based storage do not impede overall sequencing success. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By lowering data generation costs, broadening the scope of whole genome studies to include low yield DNA extracts and increasing throughput, we expect this protocol to be of significant value for a range of applications in the field of insect genomics.</span></p>',
'date' => '2023-11-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.11.24.568434v1.abstract',
'doi' => 'https://doi.org/10.1101/2023.11.24.568434',
'modified' => '2025-02-26 17:24:46',
'created' => '2025-02-26 17:24:46',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 15 => array(
'id' => '5060',
'name' => 'Therapeutic targeting of EP300/CBP by bromodomain inhibition in hematologic malignancies',
'authors' => 'Luciano Nicosia et al. ',
'description' => '<p><span>CCS1477 (inobrodib) is a potent, selective EP300/CBP bromodomain inhibitor which induces cell-cycle arrest and differentiation in hematologic malignancy model systems. In myeloid leukemia cells, it promotes rapid eviction of EP300/CBP from an enhancer subset marked by strong MYB occupancy and high H3K27 acetylation, with downregulation of the subordinate oncogenic network and redistribution to sites close to differentiation genes. In myeloma cells, CCS1477 induces eviction of EP300/CBP from </span><i>FGFR3</i><span>, the target of the common (4; 14) translocation, with redistribution away from IRF4-occupied sites to TCF3/E2A-occupied sites. In a subset of patients with relapsed or refractory disease, CCS1477 monotherapy induces differentiation responses in AML and objective responses in heavily pre-treated multiple myeloma.<span> </span></span><i>In vivo</i><span><span> </span>preclinical combination studies reveal synergistic responses to treatment with standard-of-care agents. Thus, CCS1477 exhibits encouraging preclinical and early-phase clinical activity by disrupting recruitment of EP300/CBP to enhancer networks occupied by critical transcription factors.</span></p>',
'date' => '2023-11-22',
'pmid' => 'https://www.cell.com/cancer-cell/fulltext/S1535-6108(23)00366-5',
'doi' => '10.1016/j.ccell.2023.11.001',
'modified' => '2025-02-26 17:15:25',
'created' => '2025-02-26 17:15:25',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 16 => array(
'id' => '4878',
'name' => 'ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse',
'authors' => 'Menon D.U. et al.',
'description' => '<p><span>We present evidence implicating the BAF (BRG1/BRM Associated Factor) chromatin remodeler in meiotic sex chromosome inactivation (MSCI). By immunofluorescence (IF), the putative BAF DNA binding subunit, ARID1A (AT-rich Interaction Domain 1a), appeared enriched on the male sex chromosomes during diplonema of meiosis I. The germ cell-specific depletion of ARID1A resulted in a pachynema arrest and failure to repress sex-linked genes, indicating a defective MSCI. Consistent with this defect, mutant sex chromosomes displayed an abnormal presence of elongating RNA polymerase II coupled with an overall increase in chromatin accessibility detectable by ATAC-seq. By investigating potential mechanisms underlying these anomalies, we identified a role for ARID1A in promoting the preferential enrichment of the histone variant, H3.3, on the sex chromosomes, a known hallmark of MSCI. Without ARID1A, the sex chromosomes appeared depleted of H3.3 at levels resembling autosomes. Higher resolution analyses by CUT&RUN revealed shifts in sex-linked H3.3 associations from discrete intergenic sites and broader gene-body domains to promoters in response to the loss of ARID1A. Several sex-linked sites displayed ectopic H3.3 occupancy that did not co-localize with DMC1 (DNA Meiotic Recombinase 1). This observation suggests a requirement for ARID1A in DMC1 localization to the asynapsed sex chromatids. We conclude that ARID1A-directed H3.3 localization influences meiotic sex chromosome gene regulation and DNA repair.</span></p>',
'date' => '2023-09-28',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.25.542290v2.abstract',
'doi' => 'https://doi.org/10.1101/2023.05.25.542290',
'modified' => '2023-11-10 14:53:09',
'created' => '2023-11-10 14:53:09',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 17 => array(
'id' => '5071',
'name' => 'CXCR4 signaling strength regulates hematopoietic multipotent progenitor fate through extrinsic and intrinsic mechanisms',
'authors' => 'Vincent Rondeau et al.',
'description' => '<p><span>How cell-extrinsic niche-related and cell-intrinsic cues drive lineage specification of hematopoietic multipotent progenitors (MPPs) in the bone marrow (BM) is partly understood. We show that CXCR4 signaling strength regulates localization and fate of MPPs. In mice phenocopying the BM myeloid skewing of patients with WHIM Syndrome (WS), a rare immunodeficiency caused by gain-of-function </span><em>CXCR4</em><span><span> </span>mutations, enhanced mTOR signaling and overactive Oxphos metabolism were associated with myeloid rewiring of lymphoid-primed MPPs (or MPP4). Fate decision of MPP4 was also affected by molecular changes established at the MPP1 level. Mutant MPP4 displayed altered BM localization relative to peri-arteriolar structures, suggesting that extrinsic cues contribute to their myeloid skewing. Chronic treatment with CXCR4 antagonist AMD3100 or mTOR inhibitor Rapamycin rescued lymphoid capacities of mutant MPP4, demonstrating a pivotal role for the CXCR4-mTOR axis in regulating MPP4 fate. Our study thus provides mechanistic insights into how CXCR4 signaling regulates the lymphoid potential of MPPs.</span></p>',
'date' => '2023-06-01',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.31.542899v1.abstract',
'doi' => 'https://doi.org/10.1101/2023.05.31.542899',
'modified' => '2025-02-27 11:07:18',
'created' => '2025-02-27 11:07:18',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 18 => array(
'id' => '4817',
'name' => 'YAP/BRD4-controlled ROR1 promotes tumor-initiating cells andhyperproliferation in pancreatic cancer.',
'authors' => 'Yamazaki M. et al.',
'description' => '<p><span>Tumor-initiating cells are major drivers of chemoresistance and attractive targets for cancer therapy, however, their identity in human pancreatic ductal adenocarcinoma (PDAC) and the key molecules underlying their traits remain poorly understood. Here, we show that a cellular subpopulation with partial epithelial-mesenchymal transition (EMT)-like signature marked by high expression of receptor tyrosine kinase-like orphan receptor 1 (ROR1) is the origin of heterogeneous tumor cells in PDAC. We demonstrate that ROR1 depletion suppresses tumor growth, recurrence after chemotherapy, and metastasis. Mechanistically, ROR1 induces the expression of Aurora kinase B (AURKB) by activating E2F through c-Myc to enhance PDAC proliferation. Furthermore, epigenomic analyses reveal that ROR1 is transcriptionally dependent on YAP/BRD4 binding at the enhancer region, and targeting this pathway reduces ROR1 expression and prevents PDAC growth. Collectively, our findings reveal a critical role for ROR1high cells as tumor-initiating cells and the functional importance of ROR1 in PDAC progression, thereby highlighting its therapeutic targetability.</span></p>',
'date' => '2023-04-01',
'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37096681',
'doi' => '10.15252/embj.2022112614',
'modified' => '2023-06-15 10:06:12',
'created' => '2023-06-13 21:11:31',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 19 => array(
'id' => '4742',
'name' => 'A neurodevelopmental epigenetic programme mediated bySMARCD3-DAB1-Reelin signalling is hijacked to promote medulloblastomametastasis.',
'authors' => 'Zou Han et al.',
'description' => '<p>How abnormal neurodevelopment relates to the tumour aggressiveness of medulloblastoma (MB), the most common type of embryonal tumour, remains elusive. Here we uncover a neurodevelopmental epigenomic programme that is hijacked to induce MB metastatic dissemination. Unsupervised analyses of integrated publicly available datasets with our newly generated data reveal that SMARCD3 (also known as BAF60C) regulates Disabled 1 (DAB1)-mediated Reelin signalling in Purkinje cell migration and MB metastasis by orchestrating cis-regulatory elements at the DAB1 locus. We further identify that a core set of transcription factors, enhancer of zeste homologue 2 (EZH2) and nuclear factor I X (NFIX), coordinates with the cis-regulatory elements at the SMARCD3 locus to form a chromatin hub to control SMARCD3 expression in the developing cerebellum and in metastatic MB. Increased SMARCD3 expression activates Reelin-DAB1-mediated Src kinase signalling, which results in a MB response to Src inhibition. These data deepen our understanding of how neurodevelopmental programming influences disease progression and provide a potential therapeutic option for patients with MB.</p>',
'date' => '2023-02-01',
'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36849558',
'doi' => '10.1038/s41556-023-01093-0',
'modified' => '2023-03-14 09:41:24',
'created' => '2023-03-02 17:27:08',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 20 => array(
'id' => '4660',
'name' => 'EBF1 is continuously required for stabilizing local chromatinaccessibility in pro-B cells.',
'authors' => 'Zolotarev Nikolay et al.',
'description' => '<p>The establishment of de novo chromatin accessibility in lymphoid progenitors requires the "pioneering" function of transcription factor (TF) early B cell factor 1 (EBF1), which binds to naïve chromatin and induces accessibility by recruiting the BRG1 chromatin remodeler subunit. However, it remains unclear whether the function of EBF1 is continuously required for stabilizing local chromatin accessibility. To this end, we replaced EBF1 by EBF1-FKBP in pro-B cells, allowing the rapid degradation by adding the degradation TAG13 (dTAG13) dimerizer. EBF1 degradation results in a loss of genome-wide EBF1 occupancy and EBF1-targeted BRG1 binding. Chromatin accessibility was rapidly diminished at EBF1-binding sites with a preference for sites whose occupancy requires the pioneering activity of the C-terminal domain of EBF1. Diminished chromatin accessibility correlated with altered gene expression. Thus, continuous activity of EBF1 is required for the stable maintenance of the transcriptional and epigenetic state of pro-B cells.</p>',
'date' => '2022-11-01',
'pmid' => 'https://doi.org/10.1073%2Fpnas',
'doi' => '10.1073/pnas.2210595119',
'modified' => '2023-03-07 09:07:41',
'created' => '2023-02-21 09:59:46',
'ProductsPublication' => array(
[maximum depth reached]
)
)
),
'Testimonial' => array(),
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</tr>
<tr>
<td style="width: 326px;"><span>Digitonin 1%</span></td>
<td style="width: 114px; padding-left: 30px;">0.5 µl</td>
</tr>
<tr>
<td style="width: 326px;">Tween20 10%</td>
<td style="width: 114px; padding-left: 30px;">0.5 µl</td>
</tr>
<tr>
<td style="width: 326px;">PBS</td>
<td style="width: 114px; padding-left: 30px;">16.5 µl</td>
</tr>
<tr>
<td style="width: 326px;">Nuclease-free water</td>
<td style="width: 114px; padding-left: 30px;"> 5 µl</td>
</tr>
<tr>
<td style="width: 326px;">Nuclei pellet*</td>
<td style="width: 114px;"></td>
</tr>
</tbody>
</table>
<p><em>* The number of nuclei per reaction will depend on the ATAC-seq experimental design. Successful tagmentation with the proposed protocol has been performed on 50,000 nuclei per reaction. </em></p>
<ul style="list-style-type: circle;">
<li>The reaction is then incubated 30 minutes at 37°C.</li>
<li>The tagmentation reaction can then be stopped by addition of 250 µl of DNA Binding buffer from Diagenode MicroChIP DiaPure Columns (Cat. No. C03040001).</li>
<li>The tagmented libraries can then be purified using the MicroChIP DiaPure Columns (Cat. No. C03040001), and amplified.</li>
</ul>
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(int) 0 => array(
'id' => '5041',
'name' => 'Combinatorial mapping of E3 ubiquitin ligases to their target substrates',
'authors' => 'Chase C. Suiter et al.',
'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">Developed a combinatorial assay to test E3-substrate interactions at scale</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">Identified known and unknown E3-substrate relationships across three screens</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">Assessment of<span> </span><i>in silico</i><span> </span>models points to scalable computational substrate discovery</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">Computed models of E3-substrate interactions reveal known and putative degron motifs</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">E3 ubiquitin ligases (E3s) confer specificity of protein degradation through ubiquitination of substrate proteins. Yet, the vast majority of the >600 human E3s have no known substrates. To identify proteolytic E3-substrate pairs at scale, we developed combinatorial mapping of E3 targets (COMET), a framework for testing the role of many E3s in degrading many candidate substrates within a single experiment. We applied COMET to SCF ubiquitin ligase subunits that mediate degradation of target substrates (6,716 F-box-ORF [open reading frame] combinations) and E3s that degrade short-lived transcription factors (TFs) (26,028 E3-TF combinations). Our data suggest that many E3-substrate relationships are complex rather than 1:1 associations. Finally, we leverage deep learning to predict the structural basis of E3-substrate interactions and probe the strengths and limits of such models. Looking forward, we consider the practicality of transposing this framework, i.e., computational structural prediction of all possible E3-substrate interactions, followed by multiplex experimental validation.</div>
</section>',
'date' => '2025-02-06',
'pmid' => 'https://www.cell.com/molecular-cell/fulltext/S1097-2765(25)00051-6',
'doi' => '10.1016/j.molcel.2025.01.016',
'modified' => '2025-02-10 13:35:59',
'created' => '2025-02-10 13:35:59',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 1 => array(
'id' => '5028',
'name' => 'Minimization of gene editing off-target effects by tissue restriction of expression',
'authors' => 'Nam-Gyun Kim et al.',
'description' => '<p><span>Therapeutic </span><em>in vivo</em><span><span> </span>gene editing with highly specific nucleases has the potential to revolutionize treatment for a wide range of human diseases, including genetic disorders and latent viral infections like herpes simplex virus (HSV). However, challenges regarding specificity, efficiency, delivery, and safety must be addressed before its clinical application. A key concern is the risk of off-target effects, which can cause unintended and potentially harmful genetic changes. We previously developed a curative<span> </span></span><em>in vivo</em><span><span> </span>gene editing approach to eliminate latent HSV using HSV-specific meganuclease delivered by an AAV vector. In this study, we investigate off-target effects of meganuclease by identifying potential off-target sites through GUIDE-tag analysis and assessing genetic alterations using amplicon deep sequencing in tissues from meganuclease treated mice. Our results show that meganuclease expression driven by a ubiquitous promoter leads to high off-target gene editing in the mouse liver, a non-relevant target tissue. However, restricting the meganuclease expression with a neuron-specific promoter and/or a liver-specific miRNA target sequence efficiently reduces off-target effects in both liver and trigeminal ganglia. These findings suggest that incorporation of regulatory DNA elements for tissue-specific expression in viral vectors can reduce off-target effects and improve the safety of therapeutic<span> </span></span><em>in vivo</em><span><span> </span>gene editing.</span></p>',
'date' => '2025-01-21',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2025.01.21.634017v1',
'doi' => 'https://doi.org/10.1101/2025.01.21.634017',
'modified' => '2025-01-27 14:12:10',
'created' => '2025-01-27 14:12:10',
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[maximum depth reached]
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),
(int) 2 => array(
'id' => '5002',
'name' => 'HIRA protects telomeres against R-loop-induced instability in ALT cancer cells',
'authors' => 'Michelle Lee Lynskey et al.',
'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HIRA establishes greater telomeric chromatin accessibility after ATRX-DAXX loss</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">Deposition of new H3.3 by HIRA-UBN restricts telomeric ssDNA and TERRA R-loops</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">Unresolved TERRA R-loops block new H3.3 deposition by HIRA-UBN</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">CHK1 phosphorylation of H3.3 is critical to prevent ssDNA and TERRA R-loop buildup</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">Inactivating mutations in chromatin modifiers, like the α-thalassemia/mental retardation, X-linked (ATRX)-death domain-associated protein (DAXX) chromatin remodeling/histone H3.3 deposition complex, drive the cancer-specific alternative lengthening of telomeres (ALT) pathway. Prior studies revealed that HIRA, another histone H3.3 chaperone, compensates for ATRX-DAXX loss at telomeres to sustain ALT cancer cell survival. How HIRA rescues telomeres from the consequences of ATRX-DAXX deficiency remains unclear. Here, using an assay for transposase-accessible chromatin using sequencing (ATAC-seq) and cleavage under targets and release using nuclease (CUT&RUN), we establish that HIRA-mediated deposition of new H3.3 maintains telomeric chromatin accessibility to prevent the detrimental accumulation of nucleosome-free single-stranded DNA (ssDNA) in ATRX-DAXX-deficient ALT cells. We show that the HIRA-UBN1/UBN2 complex deposits new H3.3 to prevent TERRA R-loop buildup and transcription-replication conflicts (TRCs) at telomeres. Furthermore, HIRA-mediated H3.3 incorporation into telomeric chromatin links productive ALT to the phosphorylation of serine 31, an H3.3-specific amino acid, by Chk1. Therefore, we identify a critical role for HIRA-mediated H3.3 deposition that ensures the survival of ATRX-DAXX-deficient ALT cancer cells.</div>
</section>
<section id="graphical-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name"></h2>
</section>',
'date' => '2024-11-26',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01315-9',
'doi' => '10.1016/j.celrep.2024.114964',
'modified' => '2024-11-12 09:41:40',
'created' => '2024-11-12 09:41:40',
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(int) 3 => array(
'id' => '5065',
'name' => 'Enhancing single-cell ATAC sequencing with formaldehyde fixation, cryopreservation, and multiplexing for flexible analysis',
'authors' => 'Tobias Hohl et al.',
'description' => '<p><span>The assay for transposase-accessible chromatin using sequencing (ATAC-seq) revolutionized the field of epigenetics since its emergence by providing a means to uncover chromatin dynamics and other factors affecting gene expression. The development of single-cell (sc) applications in recent years led to an even deeper understanding of cell type specific gene regulatory mechanisms. One of the major challenges while running ATAC-seq experiments, bulk or sc, is the need for freshly collected cells for successful experiments. While various freezing methods have already been tested and established for bulk and sc ATAC-seq, quality metrics for preserved cells are rather poor or dependent on sampling time when compared to fresh samples. This makes it difficult to conduct all sorts of complex experiments i.e. with multiple conditions, patients, or time course studies. Especially, accounting for batch effects can be difficult if samples need to be processed at different time points of collection. We tackled this issue by adding a fixation step prior to the freezing method. The additional fixation step improved library quality and yield data comparable to fresh samples. The workflow was also tested on multiplexed sc ATAC experiments, set-up for cost-efficient low input sample handling. Sample cross-in, typically encountered in Tn5-based multiplex approaches, were tackled with a computational procedure specifically developed for this approach.</span></p>',
'date' => '2024-11-21',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.11.20.624480v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.11.20.624480',
'modified' => '2025-02-27 10:48:39',
'created' => '2025-02-27 10:48:39',
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),
(int) 4 => array(
'id' => '5055',
'name' => 'On the identification of differentially-active transcription factors from ATAC-seq data',
'authors' => 'Felix Ezequiel Gerbaldo et al.',
'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (a chromVAR-limma workflow with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs—in our case NFkB—at the protein level.</span></p>',
'date' => '2024-10-23',
'pmid' => 'https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1011971',
'doi' => 'https://doi.org/10.1371/journal.pcbi.1011971',
'modified' => '2025-02-26 17:05:52',
'created' => '2025-02-26 17:05:52',
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),
(int) 5 => array(
'id' => '4985',
'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
'authors' => 'Alessia Bagattin et al.',
'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HNF1β mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1β partner, mediates mitosis-specific interaction with TOP1</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1β recruits TOP1 and induces DNA relaxation around bookmarked HNF1β sites</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1β mutation, found in MODY patients, disrupts the interaction with TOP1</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">HNF1β (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that HNF1β remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1β-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1β and TOP1, where a mutation, found in “maturity onset diabetes of the young” patients, disrupts their interaction. Importantly, HNF1β recruits TOP1 and induces DNA relaxation around HNF1β mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1β reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
'date' => '2024-10-08',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
'doi' => '10.1016/j.celrep.2024.114805',
'modified' => '2024-10-14 09:04:44',
'created' => '2024-10-14 09:04:44',
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),
(int) 6 => array(
'id' => '5056',
'name' => 'Rhabdomyosarcoma fusion oncoprotein initially pioneers a neural signature in vivo',
'authors' => 'Jack Kucinski et al.',
'description' => '<p><span>Fusion-positive rhabdomyosarcoma is an aggressive pediatric cancer molecularly characterized by arrested myogenesis. The defining genetic driver, PAX3::FOXO1, functions as a chimeric gain-of-function transcription factor. An incomplete understanding of PAX3::FOXO1’s in vivo epigenetic mechanisms has hindered therapeutic development. Here, we establish a PAX3::FOXO1 zebrafish injection model and semi-automated ChIP-seq normalization strategy to evaluate how PAX3::FOXO1 initially interfaces with chromatin in a developmental context. We investigated PAX3::FOXO1’s recognition of chromatin and subsequent transcriptional consequences. We find that PAX3::FOXO1 interacts with inaccessible chromatin through partial/homeobox motif recognition consistent with pioneering activity. However, PAX3::FOXO1-genome binding through a composite paired-box/homeobox motif alters chromatin accessibility and redistributes H3K27ac to activate neural transcriptional programs. We uncover neural signatures that are highly representative of clinical rhabdomyosarcoma gene expression programs that are enriched following chemotherapy. Overall, we identify partial/homeobox motif recognition as a new mode for PAX3::FOXO1 pioneer function and identify neural signatures as a potentially critical PAX3::FOXO1 tumor initiation event.</span></p>',
'date' => '2024-07-16',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.07.12.603270v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.07.12.603270',
'modified' => '2025-02-26 17:07:24',
'created' => '2025-02-26 17:07:24',
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[maximum depth reached]
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),
(int) 7 => array(
'id' => '5058',
'name' => 'CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly',
'authors' => 'Hanna Schwaemmle et al.',
'description' => '<p><span>The SWI/SNF (or BAF) complex is an essential chromatin remodeler that regulates DNA accessibility at developmental genes and enhancers. SWI/SNF subunits are among the most frequently mutated genes in cancer and neurodevelopmental disorders. These mutations are often heterozygous loss-of-function alleles, indicating a dosage-sensitive role for SWI/SNF subunits in chromatin regulation. However, the molecular mechanisms that regulate SWI/SNF subunit dosage to ensure proper complex assembly remain largely unexplored. We performed a genome-wide CRISPR KO screen, using epigenome editing in mouse embryonic stem cells, and identified </span><em>Mlf2</em><span><span> </span>and<span> </span></span><em>Rbm15</em><span><span> </span>as regulators of SWI/SNF complex activity. First, we show that MLF2, a poorly characterized chaperone protein, regulates a subset of SWI/SNF target genes by promoting chromatin remodeling activity. Next, we find that RBM15, part of the m</span><sup>6</sup><span>A RNA methylation writer complex, controls m</span><sup>6</sup><span>A modifications on specific SWI/SNF mRNAs to regulate protein levels of these subunits. Misregulation of m</span><sup>6</sup><span>A methylation causes overexpression of core SWI/SNF subunits leading to the assembly of incomplete complexes lacking the catalytic ATPase/ARP subunits. These data indicate that targeting modulators of SWI/SNF complex assembly may offer a potent therapeutic strategy for diseases associated with impaired chromatin remodeling.</span></p>',
'date' => '2024-06-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.06.25.600572v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.06.25.600572',
'modified' => '2025-02-26 17:10:53',
'created' => '2025-02-26 17:10:53',
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[maximum depth reached]
)
),
(int) 8 => array(
'id' => '5061',
'name' => 'Clock-dependent chromatin accessibility rhythms regulate circadian transcription',
'authors' => 'Ye Yuan et al.',
'description' => '<p><span>Chromatin organization plays a crucial role in gene regulation by controlling the accessibility of DNA to transcription machinery. While significant progress has been made in understanding the regulatory role of clock proteins in circadian rhythms, how chromatin organization affects circadian rhythms remains poorly understood. Here, we employed ATAC-seq (Assay for Transposase-Accessible Chromatin with Sequencing) on FAC-sorted Drosophila clock neurons to assess genome-wide chromatin accessibility at dawn and dusk over the circadian cycle. We observed significant oscillations in chromatin accessibility at promoter and enhancer regions of hundreds of genes, with enhanced accessibility either at dusk or dawn, which correlated with their peak transcriptional activity. Notably, genes with enhanced accessibility at dusk were enriched with E-box motifs, while those more accessible at dawn were enriched with VRI/PDP1-box motifs, indicating that they are regulated by the core circadian feedback loops, PER/CLK and VRI/PDP1, respectively. Further, we observed a complete loss of chromatin accessibility rhythms in </span><em>per</em><sup><em>01</em></sup><span><span> </span>null mutants, with chromatin consistently accessible at both dawn and dusk, underscoring the critical role of Period protein in driving chromatin compaction during the repression phase at dawn. Together, this study demonstrates the significant role of chromatin organization in circadian regulation, revealing how the interplay between clock proteins and chromatin structure orchestrates the precise timing of biological processes throughout the day. This work further implies that variations in chromatin accessibility might play a central role in the generation of diverse circadian gene expression patterns in clock neurons.</span></p>',
'date' => '2024-05-28',
'pmid' => 'https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1011278',
'doi' => 'https://doi.org/10.1371/journal.pgen.1011278',
'modified' => '2025-02-26 17:21:25',
'created' => '2025-02-26 17:21:25',
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[maximum depth reached]
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),
(int) 9 => array(
'id' => '5062',
'name' => 'PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites',
'authors' => 'Andrew Dimond et al.',
'description' => '<p><span>PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in </span><em>Pbk<sup>−/−</sup></em><span>preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by<span> </span></span><em>Ikzf1</em><span>,<span> </span></span><em>Ikzf3</em><span>,<span> </span></span><em>Znf131</em><span><span> </span>and<span> </span></span><em>Zbtb11</em><span>. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction.</span></p>',
'date' => '2024-04-23',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.23.590758v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.04.23.590758',
'modified' => '2025-02-26 17:22:58',
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[maximum depth reached]
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),
(int) 10 => array(
'id' => '5057',
'name' => 'Widespread impact of nucleosome remodelers on transcription at cis-regulatory elements',
'authors' => 'Benjamin J. Patty et al.',
'description' => '<p><span>Nucleosome remodeling complexes and other regulatory factors work in concert to build a chromatin environment that directs the expression of a distinct set of genes in each cell using cis-regulatory elements (CREs), such as promoters and enhancers, that drive transcription of both mRNAs and CRE-associated non-coding RNAs (ncRNAs). Two classes of CRE-associated ncRNAs include upstream antisense RNAs (uaRNAs), which are transcribed divergently from a shared mRNA promoter, and enhancer RNAs (eRNAs), which are transcribed bidirectionally from active enhancers. The complicated network of CRE regulation by nucleosome remodelers remains only partially explored, with a focus on a select, limited number of remodelers. We endeavored to elucidate a remodeler-based regulatory network governing CRE-associated transcription (mRNA, eRNA, and uaRNA) in murine embryonic stem (ES) cells to test the hypothesis that many SNF2-family nucleosome remodelers collaborate to regulate the coding and non-coding transcriptome via alteration of underlying nucleosome architecture. Using depletion followed by transient transcriptome sequencing (TT-seq), we identified thousands of misregulated mRNAs and CRE-associated ncRNAs across the remodelers examined, identifying novel contributions by understudied remodelers in the regulation of coding and non-coding transcription. Our findings suggest that mRNA and eRNA transcription are coordinately co-regulated, while mRNA and uaRNAs sharing a common promoter are independently regulated. Subsequent mechanistic studies suggest that while remodelers SRCAP and CHD8 modulate transcription through classical mechanisms such as transcription factors and histone variants, a broad set of remodelers including SMARCAL1 indirectly contribute to transcriptional regulation through maintenance of genomic stability and proper Integrator complex localization. This study systematically examines the contribution of SNF2-remodelers to the CRE-associated transcriptome, identifying at least two classes for remodeler action.</span></p>',
'date' => '2024-04-15',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.12.589208v1',
'doi' => 'https://doi.org/10.1101/2024.04.12.589208',
'modified' => '2025-02-26 17:09:18',
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(int) 11 => array(
'id' => '4926',
'name' => 'High-throughput sequencing of insect specimens with sub-optimal DNA preservation using a practical, plate-based Illumina-compatible Tn5 transposase library preparation method',
'authors' => 'Cobb L. et all.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we use a practical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs that were stored under sub-optimal conditions for DNA preservation. The samples were kept in field vehicles for extended periods of time, before long-term storage in ethanol in the freezer, or dry at room temperature. By reducing DNA input to 6ng, more samples with sub-optimal DNA yields could be processed. We matched this low DNA input with a 6-fold dilution of a commercially available tagmentation enzyme, significantly reducing library preparation costs. Costs and workload were further suppressed by direct post-amplification pooling of individual libraries. We generated medium coverage (>3-fold) genomes for 88 out of 90 specimens, with an average of approximately 10-fold coverage. While samples stored in ethanol yielded significantly less DNA compared to those which were stored dry, these samples had superior sequencing statistics, with longer sequencing reads and higher rates of endogenous DNA. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by a thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By opening opportunities for the use of sub-optimally preserved, low yield DNA extracts, we broaden the scope of whole genome studies of insect specimens. We therefore expect these results and this protocol to be valuable for a range of applications in the field of entomology.</span></p>',
'date' => '2024-03-22',
'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/38517905/',
'doi' => '10.1371/journal.pone.0300865',
'modified' => '2024-03-25 11:15:06',
'created' => '2024-03-25 11:15:06',
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(int) 12 => array(
'id' => '4923',
'name' => 'On the identification of differentially-active transcription factors from ATAC-seq data',
'authors' => 'Gerbaldo F. et al.',
'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (chromVAR-limma with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs – in our case NFkB – at the protein level.</span></p>',
'date' => '2024-03-10',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.03.06.583825v2',
'doi' => 'https://doi.org/10.1101/2024.03.06.583825',
'modified' => '2024-03-13 17:04:33',
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'name' => 'Improved metagenome assemblies through selective enrichment of bacterial genomic DNA from eukaryotic host genomic DNA using ATAC-seq',
'authors' => 'Lindsey J Cantin et al.',
'description' => '<p><span>Genomics can be used to study the complex relationships between hosts and their microbiota. Many bacteria cannot be cultured in the laboratory, making it difficult to obtain adequate amounts of bacterial DNA and to limit host DNA contamination for the construction of metagenome-assembled genomes (MAGs). For example, </span><em>Wolbachia</em><span><span> </span>is a genus of exclusively obligate intracellular bacteria that live in a wide range of arthropods and some nematodes. While<span> </span></span><em>Wolbachia</em><span><span> </span>endosymbionts are frequently described as facultative reproductive parasites in arthropods, the bacteria are obligate mutualistic endosymbionts of filarial worms. Here, we achieve 50-fold enrichment of bacterial sequences using ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) with<span> </span></span><em>Brugia malayi</em><span><span> </span>nematodes, containing<span> </span></span><em>Wolbachia</em><span><span> </span>(</span><em>w</em><span>Bm). ATAC-seq uses the Tn5 transposase to cut and attach Illumina sequencing adapters to accessible DNA lacking histones, typically thought to be open chromatin. Bacterial and mitochondrial DNA in the lysates are also cut preferentially since they lack histones, leading to the enrichment of these sequences. The benefits of this include minimal tissue input (<1 mg of tissue), a quick protocol (<4 h), low sequencing costs, less bias, correct assembly of lateral gene transfers and no prior sequence knowledge required. We assembled the<span> </span></span><em>w</em><span>Bm genome with as few as 1 million Illumina short paired-end reads with >97% coverage of the published genome, compared to only 12% coverage with the standard gDNA libraries. We found significant bacterial sequence enrichment that facilitated genome assembly in previously published ATAC-seq data sets from human cells infected with<span> </span></span><em>Mycobacterium tuberculosis</em><span><span> </span>and<span> </span></span><em>C. elegans</em><span><span> </span>contaminated with their food source, the OP50 strain of<span> </span></span><em>E. coli</em><span>. These results demonstrate the feasibility and benefits of using ATAC-seq to easily obtain bacterial genomes to aid in symbiosis, infectious disease, and microbiome research.</span></p>',
'date' => '2024-02-15',
'pmid' => 'https://pmc.ncbi.nlm.nih.gov/articles/PMC10902005/',
'doi' => '10.3389/fmicb.2024.1352378',
'modified' => '2024-11-29 11:10:24',
'created' => '2024-11-29 11:10:24',
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(int) 14 => array(
'id' => '5063',
'name' => 'A fast and inexpensive plate-based NGS library preparation method for insect genomics',
'authors' => 'Lauren Cobb et al.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we investigate a fast and economical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs stored under different conditions. Using a standardised input of 6ng DNA, library preparation costs were significantly reduced through the 6-fold dilution of a commercially available tagmentation enzyme. Costs were further suppressed by direct post-amplification pooling, skipping quality assessment of individual libraries. We find that reduced DNA yields associated with ethanol-based storage do not impede overall sequencing success. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By lowering data generation costs, broadening the scope of whole genome studies to include low yield DNA extracts and increasing throughput, we expect this protocol to be of significant value for a range of applications in the field of insect genomics.</span></p>',
'date' => '2023-11-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.11.24.568434v1.abstract',
'doi' => 'https://doi.org/10.1101/2023.11.24.568434',
'modified' => '2025-02-26 17:24:46',
'created' => '2025-02-26 17:24:46',
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(int) 15 => array(
'id' => '5060',
'name' => 'Therapeutic targeting of EP300/CBP by bromodomain inhibition in hematologic malignancies',
'authors' => 'Luciano Nicosia et al. ',
'description' => '<p><span>CCS1477 (inobrodib) is a potent, selective EP300/CBP bromodomain inhibitor which induces cell-cycle arrest and differentiation in hematologic malignancy model systems. In myeloid leukemia cells, it promotes rapid eviction of EP300/CBP from an enhancer subset marked by strong MYB occupancy and high H3K27 acetylation, with downregulation of the subordinate oncogenic network and redistribution to sites close to differentiation genes. In myeloma cells, CCS1477 induces eviction of EP300/CBP from </span><i>FGFR3</i><span>, the target of the common (4; 14) translocation, with redistribution away from IRF4-occupied sites to TCF3/E2A-occupied sites. In a subset of patients with relapsed or refractory disease, CCS1477 monotherapy induces differentiation responses in AML and objective responses in heavily pre-treated multiple myeloma.<span> </span></span><i>In vivo</i><span><span> </span>preclinical combination studies reveal synergistic responses to treatment with standard-of-care agents. Thus, CCS1477 exhibits encouraging preclinical and early-phase clinical activity by disrupting recruitment of EP300/CBP to enhancer networks occupied by critical transcription factors.</span></p>',
'date' => '2023-11-22',
'pmid' => 'https://www.cell.com/cancer-cell/fulltext/S1535-6108(23)00366-5',
'doi' => '10.1016/j.ccell.2023.11.001',
'modified' => '2025-02-26 17:15:25',
'created' => '2025-02-26 17:15:25',
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(int) 16 => array(
'id' => '4878',
'name' => 'ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse',
'authors' => 'Menon D.U. et al.',
'description' => '<p><span>We present evidence implicating the BAF (BRG1/BRM Associated Factor) chromatin remodeler in meiotic sex chromosome inactivation (MSCI). By immunofluorescence (IF), the putative BAF DNA binding subunit, ARID1A (AT-rich Interaction Domain 1a), appeared enriched on the male sex chromosomes during diplonema of meiosis I. The germ cell-specific depletion of ARID1A resulted in a pachynema arrest and failure to repress sex-linked genes, indicating a defective MSCI. Consistent with this defect, mutant sex chromosomes displayed an abnormal presence of elongating RNA polymerase II coupled with an overall increase in chromatin accessibility detectable by ATAC-seq. By investigating potential mechanisms underlying these anomalies, we identified a role for ARID1A in promoting the preferential enrichment of the histone variant, H3.3, on the sex chromosomes, a known hallmark of MSCI. Without ARID1A, the sex chromosomes appeared depleted of H3.3 at levels resembling autosomes. Higher resolution analyses by CUT&RUN revealed shifts in sex-linked H3.3 associations from discrete intergenic sites and broader gene-body domains to promoters in response to the loss of ARID1A. Several sex-linked sites displayed ectopic H3.3 occupancy that did not co-localize with DMC1 (DNA Meiotic Recombinase 1). This observation suggests a requirement for ARID1A in DMC1 localization to the asynapsed sex chromatids. We conclude that ARID1A-directed H3.3 localization influences meiotic sex chromosome gene regulation and DNA repair.</span></p>',
'date' => '2023-09-28',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.25.542290v2.abstract',
'doi' => 'https://doi.org/10.1101/2023.05.25.542290',
'modified' => '2023-11-10 14:53:09',
'created' => '2023-11-10 14:53:09',
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(int) 17 => array(
'id' => '5071',
'name' => 'CXCR4 signaling strength regulates hematopoietic multipotent progenitor fate through extrinsic and intrinsic mechanisms',
'authors' => 'Vincent Rondeau et al.',
'description' => '<p><span>How cell-extrinsic niche-related and cell-intrinsic cues drive lineage specification of hematopoietic multipotent progenitors (MPPs) in the bone marrow (BM) is partly understood. We show that CXCR4 signaling strength regulates localization and fate of MPPs. In mice phenocopying the BM myeloid skewing of patients with WHIM Syndrome (WS), a rare immunodeficiency caused by gain-of-function </span><em>CXCR4</em><span><span> </span>mutations, enhanced mTOR signaling and overactive Oxphos metabolism were associated with myeloid rewiring of lymphoid-primed MPPs (or MPP4). Fate decision of MPP4 was also affected by molecular changes established at the MPP1 level. Mutant MPP4 displayed altered BM localization relative to peri-arteriolar structures, suggesting that extrinsic cues contribute to their myeloid skewing. Chronic treatment with CXCR4 antagonist AMD3100 or mTOR inhibitor Rapamycin rescued lymphoid capacities of mutant MPP4, demonstrating a pivotal role for the CXCR4-mTOR axis in regulating MPP4 fate. Our study thus provides mechanistic insights into how CXCR4 signaling regulates the lymphoid potential of MPPs.</span></p>',
'date' => '2023-06-01',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.31.542899v1.abstract',
'doi' => 'https://doi.org/10.1101/2023.05.31.542899',
'modified' => '2025-02-27 11:07:18',
'created' => '2025-02-27 11:07:18',
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'id' => '4817',
'name' => 'YAP/BRD4-controlled ROR1 promotes tumor-initiating cells andhyperproliferation in pancreatic cancer.',
'authors' => 'Yamazaki M. et al.',
'description' => '<p><span>Tumor-initiating cells are major drivers of chemoresistance and attractive targets for cancer therapy, however, their identity in human pancreatic ductal adenocarcinoma (PDAC) and the key molecules underlying their traits remain poorly understood. Here, we show that a cellular subpopulation with partial epithelial-mesenchymal transition (EMT)-like signature marked by high expression of receptor tyrosine kinase-like orphan receptor 1 (ROR1) is the origin of heterogeneous tumor cells in PDAC. We demonstrate that ROR1 depletion suppresses tumor growth, recurrence after chemotherapy, and metastasis. Mechanistically, ROR1 induces the expression of Aurora kinase B (AURKB) by activating E2F through c-Myc to enhance PDAC proliferation. Furthermore, epigenomic analyses reveal that ROR1 is transcriptionally dependent on YAP/BRD4 binding at the enhancer region, and targeting this pathway reduces ROR1 expression and prevents PDAC growth. Collectively, our findings reveal a critical role for ROR1high cells as tumor-initiating cells and the functional importance of ROR1 in PDAC progression, thereby highlighting its therapeutic targetability.</span></p>',
'date' => '2023-04-01',
'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37096681',
'doi' => '10.15252/embj.2022112614',
'modified' => '2023-06-15 10:06:12',
'created' => '2023-06-13 21:11:31',
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(int) 19 => array(
'id' => '4742',
'name' => 'A neurodevelopmental epigenetic programme mediated bySMARCD3-DAB1-Reelin signalling is hijacked to promote medulloblastomametastasis.',
'authors' => 'Zou Han et al.',
'description' => '<p>How abnormal neurodevelopment relates to the tumour aggressiveness of medulloblastoma (MB), the most common type of embryonal tumour, remains elusive. Here we uncover a neurodevelopmental epigenomic programme that is hijacked to induce MB metastatic dissemination. Unsupervised analyses of integrated publicly available datasets with our newly generated data reveal that SMARCD3 (also known as BAF60C) regulates Disabled 1 (DAB1)-mediated Reelin signalling in Purkinje cell migration and MB metastasis by orchestrating cis-regulatory elements at the DAB1 locus. We further identify that a core set of transcription factors, enhancer of zeste homologue 2 (EZH2) and nuclear factor I X (NFIX), coordinates with the cis-regulatory elements at the SMARCD3 locus to form a chromatin hub to control SMARCD3 expression in the developing cerebellum and in metastatic MB. Increased SMARCD3 expression activates Reelin-DAB1-mediated Src kinase signalling, which results in a MB response to Src inhibition. These data deepen our understanding of how neurodevelopmental programming influences disease progression and provide a potential therapeutic option for patients with MB.</p>',
'date' => '2023-02-01',
'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36849558',
'doi' => '10.1038/s41556-023-01093-0',
'modified' => '2023-03-14 09:41:24',
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'id' => '4660',
'name' => 'EBF1 is continuously required for stabilizing local chromatinaccessibility in pro-B cells.',
'authors' => 'Zolotarev Nikolay et al.',
'description' => '<p>The establishment of de novo chromatin accessibility in lymphoid progenitors requires the "pioneering" function of transcription factor (TF) early B cell factor 1 (EBF1), which binds to naïve chromatin and induces accessibility by recruiting the BRG1 chromatin remodeler subunit. However, it remains unclear whether the function of EBF1 is continuously required for stabilizing local chromatin accessibility. To this end, we replaced EBF1 by EBF1-FKBP in pro-B cells, allowing the rapid degradation by adding the degradation TAG13 (dTAG13) dimerizer. EBF1 degradation results in a loss of genome-wide EBF1 occupancy and EBF1-targeted BRG1 binding. Chromatin accessibility was rapidly diminished at EBF1-binding sites with a preference for sites whose occupancy requires the pioneering activity of the C-terminal domain of EBF1. Diminished chromatin accessibility correlated with altered gene expression. Thus, continuous activity of EBF1 is required for the stable maintenance of the transcriptional and epigenetic state of pro-B cells.</p>',
'date' => '2022-11-01',
'pmid' => 'https://doi.org/10.1073%2Fpnas',
'doi' => '10.1073/pnas.2210595119',
'modified' => '2023-03-07 09:07:41',
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<p>Diagenode <strong>Tagmentation Buffer (2x)</strong> is the recommended reagent to perform any tagmentation reactions. It can be used in combination with Diagenode <a href="https://www.diagenode.com/en/p/tagmentase-loaded-30">Tagmentase (Tn5 transposase)</a> on DNA or chromatin samples, as half of the total volume reaction like in ATAC-seq protocol.</p>
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'info1' => '<p><span style="text-decoration: underline;">ATAC-seq experiments: </span></p>
<ul style="list-style-type: circle;">
<li>After cell lysis and nuclei isolation, the nuclei pellets can be incubated with the following mix for 1 reaction:</li>
</ul>
<table style="width: 447px;">
<tbody>
<tr>
<td style="width: 326px;">Tagmentation Buffer (2x)</td>
<td style="width: 114px; padding-left: 30px;">25 µl</td>
</tr>
<tr>
<td style="width: 326px;">Tagmentase loaded</td>
<td style="width: 114px; padding-left: 30px;">2.5 µl</td>
</tr>
<tr>
<td style="width: 326px;"><span>Digitonin 1%</span></td>
<td style="width: 114px; padding-left: 30px;">0.5 µl</td>
</tr>
<tr>
<td style="width: 326px;">Tween20 10%</td>
<td style="width: 114px; padding-left: 30px;">0.5 µl</td>
</tr>
<tr>
<td style="width: 326px;">PBS</td>
<td style="width: 114px; padding-left: 30px;">16.5 µl</td>
</tr>
<tr>
<td style="width: 326px;">Nuclease-free water</td>
<td style="width: 114px; padding-left: 30px;"> 5 µl</td>
</tr>
<tr>
<td style="width: 326px;">Nuclei pellet*</td>
<td style="width: 114px;"></td>
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<div id="abspara0010" role="paragraph">E3 ubiquitin ligases (E3s) confer specificity of protein degradation through ubiquitination of substrate proteins. Yet, the vast majority of the >600 human E3s have no known substrates. To identify proteolytic E3-substrate pairs at scale, we developed combinatorial mapping of E3 targets (COMET), a framework for testing the role of many E3s in degrading many candidate substrates within a single experiment. We applied COMET to SCF ubiquitin ligase subunits that mediate degradation of target substrates (6,716 F-box-ORF [open reading frame] combinations) and E3s that degrade short-lived transcription factors (TFs) (26,028 E3-TF combinations). Our data suggest that many E3-substrate relationships are complex rather than 1:1 associations. Finally, we leverage deep learning to predict the structural basis of E3-substrate interactions and probe the strengths and limits of such models. Looking forward, we consider the practicality of transposing this framework, i.e., computational structural prediction of all possible E3-substrate interactions, followed by multiplex experimental validation.</div>
</section>',
'date' => '2025-02-06',
'pmid' => 'https://www.cell.com/molecular-cell/fulltext/S1097-2765(25)00051-6',
'doi' => '10.1016/j.molcel.2025.01.016',
'modified' => '2025-02-10 13:35:59',
'created' => '2025-02-10 13:35:59',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 1 => array(
'id' => '5028',
'name' => 'Minimization of gene editing off-target effects by tissue restriction of expression',
'authors' => 'Nam-Gyun Kim et al.',
'description' => '<p><span>Therapeutic </span><em>in vivo</em><span><span> </span>gene editing with highly specific nucleases has the potential to revolutionize treatment for a wide range of human diseases, including genetic disorders and latent viral infections like herpes simplex virus (HSV). However, challenges regarding specificity, efficiency, delivery, and safety must be addressed before its clinical application. A key concern is the risk of off-target effects, which can cause unintended and potentially harmful genetic changes. We previously developed a curative<span> </span></span><em>in vivo</em><span><span> </span>gene editing approach to eliminate latent HSV using HSV-specific meganuclease delivered by an AAV vector. In this study, we investigate off-target effects of meganuclease by identifying potential off-target sites through GUIDE-tag analysis and assessing genetic alterations using amplicon deep sequencing in tissues from meganuclease treated mice. Our results show that meganuclease expression driven by a ubiquitous promoter leads to high off-target gene editing in the mouse liver, a non-relevant target tissue. However, restricting the meganuclease expression with a neuron-specific promoter and/or a liver-specific miRNA target sequence efficiently reduces off-target effects in both liver and trigeminal ganglia. These findings suggest that incorporation of regulatory DNA elements for tissue-specific expression in viral vectors can reduce off-target effects and improve the safety of therapeutic<span> </span></span><em>in vivo</em><span><span> </span>gene editing.</span></p>',
'date' => '2025-01-21',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2025.01.21.634017v1',
'doi' => 'https://doi.org/10.1101/2025.01.21.634017',
'modified' => '2025-01-27 14:12:10',
'created' => '2025-01-27 14:12:10',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 2 => array(
'id' => '5002',
'name' => 'HIRA protects telomeres against R-loop-induced instability in ALT cancer cells',
'authors' => 'Michelle Lee Lynskey et al.',
'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HIRA establishes greater telomeric chromatin accessibility after ATRX-DAXX loss</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">Deposition of new H3.3 by HIRA-UBN restricts telomeric ssDNA and TERRA R-loops</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">Unresolved TERRA R-loops block new H3.3 deposition by HIRA-UBN</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">CHK1 phosphorylation of H3.3 is critical to prevent ssDNA and TERRA R-loop buildup</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">Inactivating mutations in chromatin modifiers, like the α-thalassemia/mental retardation, X-linked (ATRX)-death domain-associated protein (DAXX) chromatin remodeling/histone H3.3 deposition complex, drive the cancer-specific alternative lengthening of telomeres (ALT) pathway. Prior studies revealed that HIRA, another histone H3.3 chaperone, compensates for ATRX-DAXX loss at telomeres to sustain ALT cancer cell survival. How HIRA rescues telomeres from the consequences of ATRX-DAXX deficiency remains unclear. Here, using an assay for transposase-accessible chromatin using sequencing (ATAC-seq) and cleavage under targets and release using nuclease (CUT&RUN), we establish that HIRA-mediated deposition of new H3.3 maintains telomeric chromatin accessibility to prevent the detrimental accumulation of nucleosome-free single-stranded DNA (ssDNA) in ATRX-DAXX-deficient ALT cells. We show that the HIRA-UBN1/UBN2 complex deposits new H3.3 to prevent TERRA R-loop buildup and transcription-replication conflicts (TRCs) at telomeres. Furthermore, HIRA-mediated H3.3 incorporation into telomeric chromatin links productive ALT to the phosphorylation of serine 31, an H3.3-specific amino acid, by Chk1. Therefore, we identify a critical role for HIRA-mediated H3.3 deposition that ensures the survival of ATRX-DAXX-deficient ALT cancer cells.</div>
</section>
<section id="graphical-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name"></h2>
</section>',
'date' => '2024-11-26',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01315-9',
'doi' => '10.1016/j.celrep.2024.114964',
'modified' => '2024-11-12 09:41:40',
'created' => '2024-11-12 09:41:40',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 3 => array(
'id' => '5065',
'name' => 'Enhancing single-cell ATAC sequencing with formaldehyde fixation, cryopreservation, and multiplexing for flexible analysis',
'authors' => 'Tobias Hohl et al.',
'description' => '<p><span>The assay for transposase-accessible chromatin using sequencing (ATAC-seq) revolutionized the field of epigenetics since its emergence by providing a means to uncover chromatin dynamics and other factors affecting gene expression. The development of single-cell (sc) applications in recent years led to an even deeper understanding of cell type specific gene regulatory mechanisms. One of the major challenges while running ATAC-seq experiments, bulk or sc, is the need for freshly collected cells for successful experiments. While various freezing methods have already been tested and established for bulk and sc ATAC-seq, quality metrics for preserved cells are rather poor or dependent on sampling time when compared to fresh samples. This makes it difficult to conduct all sorts of complex experiments i.e. with multiple conditions, patients, or time course studies. Especially, accounting for batch effects can be difficult if samples need to be processed at different time points of collection. We tackled this issue by adding a fixation step prior to the freezing method. The additional fixation step improved library quality and yield data comparable to fresh samples. The workflow was also tested on multiplexed sc ATAC experiments, set-up for cost-efficient low input sample handling. Sample cross-in, typically encountered in Tn5-based multiplex approaches, were tackled with a computational procedure specifically developed for this approach.</span></p>',
'date' => '2024-11-21',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.11.20.624480v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.11.20.624480',
'modified' => '2025-02-27 10:48:39',
'created' => '2025-02-27 10:48:39',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 4 => array(
'id' => '5055',
'name' => 'On the identification of differentially-active transcription factors from ATAC-seq data',
'authors' => 'Felix Ezequiel Gerbaldo et al.',
'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (a chromVAR-limma workflow with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs—in our case NFkB—at the protein level.</span></p>',
'date' => '2024-10-23',
'pmid' => 'https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1011971',
'doi' => 'https://doi.org/10.1371/journal.pcbi.1011971',
'modified' => '2025-02-26 17:05:52',
'created' => '2025-02-26 17:05:52',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 5 => array(
'id' => '4985',
'name' => 'HNF1β bookmarking involves Topoisomerase 1 activation and DNA topology relaxation in mitotic chromatin',
'authors' => 'Alessia Bagattin et al.',
'description' => '<section id="author-highlights-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Highlights</h2>
<div id="abspara0020" role="paragraph">
<div id="ulist0010" role="list">
<div id="u0010" role="listitem">
<div class="content">
<div id="p0010" role="paragraph">HNF1β mitotic site binding is preserved with a specific methanol/formaldehyde ChIP</div>
</div>
</div>
<div id="u0015" role="listitem">
<div class="content">
<div id="p0015" role="paragraph">BTBD2, an HNF1β partner, mediates mitosis-specific interaction with TOP1</div>
</div>
</div>
<div id="u0020" role="listitem">
<div class="content">
<div id="p0020" role="paragraph">HNF1β recruits TOP1 and induces DNA relaxation around bookmarked HNF1β sites</div>
</div>
</div>
<div id="u0025" role="listitem">
<div class="content">
<div id="p0025" role="paragraph">An HNF1β mutation, found in MODY patients, disrupts the interaction with TOP1</div>
</div>
</div>
</div>
</div>
</section>
<section id="author-abstract" property="abstract" typeof="Text" role="doc-abstract">
<h2 property="name">Summary</h2>
<div id="abspara0010" role="paragraph">HNF1β (<i>HNF1B</i>) is a transcription factor frequently mutated in patients with developmental renal disease. It binds to mitotic chromatin and reactivates gene expression after mitosis, a phenomenon referred to as bookmarking. Using a crosslinking method that circumvents the artifacts of formaldehyde, we demonstrate that HNF1β remains associated with chromatin in a sequence-specific way in both interphase and mitosis. We identify an HNF1β-interacting protein, BTBD2, that enables the interaction and activation of Topoisomerase 1 (TOP1) exclusively during mitosis. Our study identifies a shared microhomology domain between HNF1β and TOP1, where a mutation, found in “maturity onset diabetes of the young” patients, disrupts their interaction. Importantly, HNF1β recruits TOP1 and induces DNA relaxation around HNF1β mitotic chromatin sites, elucidating its crucial role in chromatin remodeling and gene reactivation after mitotic exit. These findings shed light on how HNF1β reactivates target gene expression after mitosis, providing insights into its crucial role in maintenance of cellular identity.</div>
</section>',
'date' => '2024-10-08',
'pmid' => 'https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01156-2',
'doi' => '10.1016/j.celrep.2024.114805',
'modified' => '2024-10-14 09:04:44',
'created' => '2024-10-14 09:04:44',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 6 => array(
'id' => '5056',
'name' => 'Rhabdomyosarcoma fusion oncoprotein initially pioneers a neural signature in vivo',
'authors' => 'Jack Kucinski et al.',
'description' => '<p><span>Fusion-positive rhabdomyosarcoma is an aggressive pediatric cancer molecularly characterized by arrested myogenesis. The defining genetic driver, PAX3::FOXO1, functions as a chimeric gain-of-function transcription factor. An incomplete understanding of PAX3::FOXO1’s in vivo epigenetic mechanisms has hindered therapeutic development. Here, we establish a PAX3::FOXO1 zebrafish injection model and semi-automated ChIP-seq normalization strategy to evaluate how PAX3::FOXO1 initially interfaces with chromatin in a developmental context. We investigated PAX3::FOXO1’s recognition of chromatin and subsequent transcriptional consequences. We find that PAX3::FOXO1 interacts with inaccessible chromatin through partial/homeobox motif recognition consistent with pioneering activity. However, PAX3::FOXO1-genome binding through a composite paired-box/homeobox motif alters chromatin accessibility and redistributes H3K27ac to activate neural transcriptional programs. We uncover neural signatures that are highly representative of clinical rhabdomyosarcoma gene expression programs that are enriched following chemotherapy. Overall, we identify partial/homeobox motif recognition as a new mode for PAX3::FOXO1 pioneer function and identify neural signatures as a potentially critical PAX3::FOXO1 tumor initiation event.</span></p>',
'date' => '2024-07-16',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.07.12.603270v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.07.12.603270',
'modified' => '2025-02-26 17:07:24',
'created' => '2025-02-26 17:07:24',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 7 => array(
'id' => '5058',
'name' => 'CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly',
'authors' => 'Hanna Schwaemmle et al.',
'description' => '<p><span>The SWI/SNF (or BAF) complex is an essential chromatin remodeler that regulates DNA accessibility at developmental genes and enhancers. SWI/SNF subunits are among the most frequently mutated genes in cancer and neurodevelopmental disorders. These mutations are often heterozygous loss-of-function alleles, indicating a dosage-sensitive role for SWI/SNF subunits in chromatin regulation. However, the molecular mechanisms that regulate SWI/SNF subunit dosage to ensure proper complex assembly remain largely unexplored. We performed a genome-wide CRISPR KO screen, using epigenome editing in mouse embryonic stem cells, and identified </span><em>Mlf2</em><span><span> </span>and<span> </span></span><em>Rbm15</em><span><span> </span>as regulators of SWI/SNF complex activity. First, we show that MLF2, a poorly characterized chaperone protein, regulates a subset of SWI/SNF target genes by promoting chromatin remodeling activity. Next, we find that RBM15, part of the m</span><sup>6</sup><span>A RNA methylation writer complex, controls m</span><sup>6</sup><span>A modifications on specific SWI/SNF mRNAs to regulate protein levels of these subunits. Misregulation of m</span><sup>6</sup><span>A methylation causes overexpression of core SWI/SNF subunits leading to the assembly of incomplete complexes lacking the catalytic ATPase/ARP subunits. These data indicate that targeting modulators of SWI/SNF complex assembly may offer a potent therapeutic strategy for diseases associated with impaired chromatin remodeling.</span></p>',
'date' => '2024-06-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.06.25.600572v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.06.25.600572',
'modified' => '2025-02-26 17:10:53',
'created' => '2025-02-26 17:10:53',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 8 => array(
'id' => '5061',
'name' => 'Clock-dependent chromatin accessibility rhythms regulate circadian transcription',
'authors' => 'Ye Yuan et al.',
'description' => '<p><span>Chromatin organization plays a crucial role in gene regulation by controlling the accessibility of DNA to transcription machinery. While significant progress has been made in understanding the regulatory role of clock proteins in circadian rhythms, how chromatin organization affects circadian rhythms remains poorly understood. Here, we employed ATAC-seq (Assay for Transposase-Accessible Chromatin with Sequencing) on FAC-sorted Drosophila clock neurons to assess genome-wide chromatin accessibility at dawn and dusk over the circadian cycle. We observed significant oscillations in chromatin accessibility at promoter and enhancer regions of hundreds of genes, with enhanced accessibility either at dusk or dawn, which correlated with their peak transcriptional activity. Notably, genes with enhanced accessibility at dusk were enriched with E-box motifs, while those more accessible at dawn were enriched with VRI/PDP1-box motifs, indicating that they are regulated by the core circadian feedback loops, PER/CLK and VRI/PDP1, respectively. Further, we observed a complete loss of chromatin accessibility rhythms in </span><em>per</em><sup><em>01</em></sup><span><span> </span>null mutants, with chromatin consistently accessible at both dawn and dusk, underscoring the critical role of Period protein in driving chromatin compaction during the repression phase at dawn. Together, this study demonstrates the significant role of chromatin organization in circadian regulation, revealing how the interplay between clock proteins and chromatin structure orchestrates the precise timing of biological processes throughout the day. This work further implies that variations in chromatin accessibility might play a central role in the generation of diverse circadian gene expression patterns in clock neurons.</span></p>',
'date' => '2024-05-28',
'pmid' => 'https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1011278',
'doi' => 'https://doi.org/10.1371/journal.pgen.1011278',
'modified' => '2025-02-26 17:21:25',
'created' => '2025-02-26 17:21:25',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 9 => array(
'id' => '5062',
'name' => 'PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites',
'authors' => 'Andrew Dimond et al.',
'description' => '<p><span>PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in </span><em>Pbk<sup>−/−</sup></em><span>preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by<span> </span></span><em>Ikzf1</em><span>,<span> </span></span><em>Ikzf3</em><span>,<span> </span></span><em>Znf131</em><span><span> </span>and<span> </span></span><em>Zbtb11</em><span>. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction.</span></p>',
'date' => '2024-04-23',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.23.590758v1.abstract',
'doi' => 'https://doi.org/10.1101/2024.04.23.590758',
'modified' => '2025-02-26 17:22:58',
'created' => '2025-02-26 17:22:58',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 10 => array(
'id' => '5057',
'name' => 'Widespread impact of nucleosome remodelers on transcription at cis-regulatory elements',
'authors' => 'Benjamin J. Patty et al.',
'description' => '<p><span>Nucleosome remodeling complexes and other regulatory factors work in concert to build a chromatin environment that directs the expression of a distinct set of genes in each cell using cis-regulatory elements (CREs), such as promoters and enhancers, that drive transcription of both mRNAs and CRE-associated non-coding RNAs (ncRNAs). Two classes of CRE-associated ncRNAs include upstream antisense RNAs (uaRNAs), which are transcribed divergently from a shared mRNA promoter, and enhancer RNAs (eRNAs), which are transcribed bidirectionally from active enhancers. The complicated network of CRE regulation by nucleosome remodelers remains only partially explored, with a focus on a select, limited number of remodelers. We endeavored to elucidate a remodeler-based regulatory network governing CRE-associated transcription (mRNA, eRNA, and uaRNA) in murine embryonic stem (ES) cells to test the hypothesis that many SNF2-family nucleosome remodelers collaborate to regulate the coding and non-coding transcriptome via alteration of underlying nucleosome architecture. Using depletion followed by transient transcriptome sequencing (TT-seq), we identified thousands of misregulated mRNAs and CRE-associated ncRNAs across the remodelers examined, identifying novel contributions by understudied remodelers in the regulation of coding and non-coding transcription. Our findings suggest that mRNA and eRNA transcription are coordinately co-regulated, while mRNA and uaRNAs sharing a common promoter are independently regulated. Subsequent mechanistic studies suggest that while remodelers SRCAP and CHD8 modulate transcription through classical mechanisms such as transcription factors and histone variants, a broad set of remodelers including SMARCAL1 indirectly contribute to transcriptional regulation through maintenance of genomic stability and proper Integrator complex localization. This study systematically examines the contribution of SNF2-remodelers to the CRE-associated transcriptome, identifying at least two classes for remodeler action.</span></p>',
'date' => '2024-04-15',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.04.12.589208v1',
'doi' => 'https://doi.org/10.1101/2024.04.12.589208',
'modified' => '2025-02-26 17:09:18',
'created' => '2025-02-26 17:09:18',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 11 => array(
'id' => '4926',
'name' => 'High-throughput sequencing of insect specimens with sub-optimal DNA preservation using a practical, plate-based Illumina-compatible Tn5 transposase library preparation method',
'authors' => 'Cobb L. et all.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we use a practical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs that were stored under sub-optimal conditions for DNA preservation. The samples were kept in field vehicles for extended periods of time, before long-term storage in ethanol in the freezer, or dry at room temperature. By reducing DNA input to 6ng, more samples with sub-optimal DNA yields could be processed. We matched this low DNA input with a 6-fold dilution of a commercially available tagmentation enzyme, significantly reducing library preparation costs. Costs and workload were further suppressed by direct post-amplification pooling of individual libraries. We generated medium coverage (>3-fold) genomes for 88 out of 90 specimens, with an average of approximately 10-fold coverage. While samples stored in ethanol yielded significantly less DNA compared to those which were stored dry, these samples had superior sequencing statistics, with longer sequencing reads and higher rates of endogenous DNA. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by a thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By opening opportunities for the use of sub-optimally preserved, low yield DNA extracts, we broaden the scope of whole genome studies of insect specimens. We therefore expect these results and this protocol to be valuable for a range of applications in the field of entomology.</span></p>',
'date' => '2024-03-22',
'pmid' => 'https://pubmed.ncbi.nlm.nih.gov/38517905/',
'doi' => '10.1371/journal.pone.0300865',
'modified' => '2024-03-25 11:15:06',
'created' => '2024-03-25 11:15:06',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 12 => array(
'id' => '4923',
'name' => 'On the identification of differentially-active transcription factors from ATAC-seq data',
'authors' => 'Gerbaldo F. et al.',
'description' => '<p><span>ATAC-seq has emerged as a rich epigenome profiling technique, and is commonly used to identify Transcription Factors (TFs) underlying given phenomena. A number of methods can be used to identify differentially-active TFs through the accessibility of their DNA-binding motif, however little is known on the best approaches for doing so. Here we benchmark several such methods using a combination of curated datasets with various forms of short-term perturbations on known TFs, as well as semi-simulations. We include both methods specifically designed for this type of data as well as some that can be repurposed for it. We also investigate variations to these methods, and identify three particularly promising approaches (chromVAR-limma with critical adjustments, monaLisa and a combination of GC smooth quantile normalization and multivariate modeling). We further investigate the specific use of nucleosome-free fragments, the combination of top methods, and the impact of technical variation. Finally, we illustrate the use of the top methods on a novel dataset to characterize the impact on DNA accessibility of TRAnscription Factor TArgeting Chimeras (TRAFTAC), which can deplete TFs – in our case NFkB – at the protein level.</span></p>',
'date' => '2024-03-10',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2024.03.06.583825v2',
'doi' => 'https://doi.org/10.1101/2024.03.06.583825',
'modified' => '2024-03-13 17:04:33',
'created' => '2024-03-13 17:04:33',
'ProductsPublication' => array(
[maximum depth reached]
)
),
(int) 13 => array(
'id' => '5003',
'name' => 'Improved metagenome assemblies through selective enrichment of bacterial genomic DNA from eukaryotic host genomic DNA using ATAC-seq',
'authors' => 'Lindsey J Cantin et al.',
'description' => '<p><span>Genomics can be used to study the complex relationships between hosts and their microbiota. Many bacteria cannot be cultured in the laboratory, making it difficult to obtain adequate amounts of bacterial DNA and to limit host DNA contamination for the construction of metagenome-assembled genomes (MAGs). For example, </span><em>Wolbachia</em><span><span> </span>is a genus of exclusively obligate intracellular bacteria that live in a wide range of arthropods and some nematodes. While<span> </span></span><em>Wolbachia</em><span><span> </span>endosymbionts are frequently described as facultative reproductive parasites in arthropods, the bacteria are obligate mutualistic endosymbionts of filarial worms. Here, we achieve 50-fold enrichment of bacterial sequences using ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) with<span> </span></span><em>Brugia malayi</em><span><span> </span>nematodes, containing<span> </span></span><em>Wolbachia</em><span><span> </span>(</span><em>w</em><span>Bm). ATAC-seq uses the Tn5 transposase to cut and attach Illumina sequencing adapters to accessible DNA lacking histones, typically thought to be open chromatin. Bacterial and mitochondrial DNA in the lysates are also cut preferentially since they lack histones, leading to the enrichment of these sequences. The benefits of this include minimal tissue input (<1 mg of tissue), a quick protocol (<4 h), low sequencing costs, less bias, correct assembly of lateral gene transfers and no prior sequence knowledge required. We assembled the<span> </span></span><em>w</em><span>Bm genome with as few as 1 million Illumina short paired-end reads with >97% coverage of the published genome, compared to only 12% coverage with the standard gDNA libraries. We found significant bacterial sequence enrichment that facilitated genome assembly in previously published ATAC-seq data sets from human cells infected with<span> </span></span><em>Mycobacterium tuberculosis</em><span><span> </span>and<span> </span></span><em>C. elegans</em><span><span> </span>contaminated with their food source, the OP50 strain of<span> </span></span><em>E. coli</em><span>. These results demonstrate the feasibility and benefits of using ATAC-seq to easily obtain bacterial genomes to aid in symbiosis, infectious disease, and microbiome research.</span></p>',
'date' => '2024-02-15',
'pmid' => 'https://pmc.ncbi.nlm.nih.gov/articles/PMC10902005/',
'doi' => '10.3389/fmicb.2024.1352378',
'modified' => '2024-11-29 11:10:24',
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'id' => '5063',
'name' => 'A fast and inexpensive plate-based NGS library preparation method for insect genomics',
'authors' => 'Lauren Cobb et al.',
'description' => '<p><span>Entomological sampling and storage conditions often prioritise efficiency, practicality and conservation of morphological characteristics, and may therefore be suboptimal for DNA preservation. This practice can impact downstream molecular applications, such as the generation of high-throughput genomic libraries, which often requires substantial DNA input amounts. Here, we investigate a fast and economical Tn5 transposase tagmentation-based library preparation method optimised for 96-well plates and low yield DNA extracts from insect legs stored under different conditions. Using a standardised input of 6ng DNA, library preparation costs were significantly reduced through the 6-fold dilution of a commercially available tagmentation enzyme. Costs were further suppressed by direct post-amplification pooling, skipping quality assessment of individual libraries. We find that reduced DNA yields associated with ethanol-based storage do not impede overall sequencing success. Furthermore, we find that the efficiency of tagmentation-based library preparation can be improved by thorough post-amplification bead clean-up which selects against both short and large DNA fragments. By lowering data generation costs, broadening the scope of whole genome studies to include low yield DNA extracts and increasing throughput, we expect this protocol to be of significant value for a range of applications in the field of insect genomics.</span></p>',
'date' => '2023-11-25',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.11.24.568434v1.abstract',
'doi' => 'https://doi.org/10.1101/2023.11.24.568434',
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'name' => 'Therapeutic targeting of EP300/CBP by bromodomain inhibition in hematologic malignancies',
'authors' => 'Luciano Nicosia et al. ',
'description' => '<p><span>CCS1477 (inobrodib) is a potent, selective EP300/CBP bromodomain inhibitor which induces cell-cycle arrest and differentiation in hematologic malignancy model systems. In myeloid leukemia cells, it promotes rapid eviction of EP300/CBP from an enhancer subset marked by strong MYB occupancy and high H3K27 acetylation, with downregulation of the subordinate oncogenic network and redistribution to sites close to differentiation genes. In myeloma cells, CCS1477 induces eviction of EP300/CBP from </span><i>FGFR3</i><span>, the target of the common (4; 14) translocation, with redistribution away from IRF4-occupied sites to TCF3/E2A-occupied sites. In a subset of patients with relapsed or refractory disease, CCS1477 monotherapy induces differentiation responses in AML and objective responses in heavily pre-treated multiple myeloma.<span> </span></span><i>In vivo</i><span><span> </span>preclinical combination studies reveal synergistic responses to treatment with standard-of-care agents. Thus, CCS1477 exhibits encouraging preclinical and early-phase clinical activity by disrupting recruitment of EP300/CBP to enhancer networks occupied by critical transcription factors.</span></p>',
'date' => '2023-11-22',
'pmid' => 'https://www.cell.com/cancer-cell/fulltext/S1535-6108(23)00366-5',
'doi' => '10.1016/j.ccell.2023.11.001',
'modified' => '2025-02-26 17:15:25',
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'id' => '4878',
'name' => 'ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse',
'authors' => 'Menon D.U. et al.',
'description' => '<p><span>We present evidence implicating the BAF (BRG1/BRM Associated Factor) chromatin remodeler in meiotic sex chromosome inactivation (MSCI). By immunofluorescence (IF), the putative BAF DNA binding subunit, ARID1A (AT-rich Interaction Domain 1a), appeared enriched on the male sex chromosomes during diplonema of meiosis I. The germ cell-specific depletion of ARID1A resulted in a pachynema arrest and failure to repress sex-linked genes, indicating a defective MSCI. Consistent with this defect, mutant sex chromosomes displayed an abnormal presence of elongating RNA polymerase II coupled with an overall increase in chromatin accessibility detectable by ATAC-seq. By investigating potential mechanisms underlying these anomalies, we identified a role for ARID1A in promoting the preferential enrichment of the histone variant, H3.3, on the sex chromosomes, a known hallmark of MSCI. Without ARID1A, the sex chromosomes appeared depleted of H3.3 at levels resembling autosomes. Higher resolution analyses by CUT&RUN revealed shifts in sex-linked H3.3 associations from discrete intergenic sites and broader gene-body domains to promoters in response to the loss of ARID1A. Several sex-linked sites displayed ectopic H3.3 occupancy that did not co-localize with DMC1 (DNA Meiotic Recombinase 1). This observation suggests a requirement for ARID1A in DMC1 localization to the asynapsed sex chromatids. We conclude that ARID1A-directed H3.3 localization influences meiotic sex chromosome gene regulation and DNA repair.</span></p>',
'date' => '2023-09-28',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.25.542290v2.abstract',
'doi' => 'https://doi.org/10.1101/2023.05.25.542290',
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'description' => '<p><span>How cell-extrinsic niche-related and cell-intrinsic cues drive lineage specification of hematopoietic multipotent progenitors (MPPs) in the bone marrow (BM) is partly understood. We show that CXCR4 signaling strength regulates localization and fate of MPPs. In mice phenocopying the BM myeloid skewing of patients with WHIM Syndrome (WS), a rare immunodeficiency caused by gain-of-function </span><em>CXCR4</em><span><span> </span>mutations, enhanced mTOR signaling and overactive Oxphos metabolism were associated with myeloid rewiring of lymphoid-primed MPPs (or MPP4). Fate decision of MPP4 was also affected by molecular changes established at the MPP1 level. Mutant MPP4 displayed altered BM localization relative to peri-arteriolar structures, suggesting that extrinsic cues contribute to their myeloid skewing. Chronic treatment with CXCR4 antagonist AMD3100 or mTOR inhibitor Rapamycin rescued lymphoid capacities of mutant MPP4, demonstrating a pivotal role for the CXCR4-mTOR axis in regulating MPP4 fate. Our study thus provides mechanistic insights into how CXCR4 signaling regulates the lymphoid potential of MPPs.</span></p>',
'date' => '2023-06-01',
'pmid' => 'https://www.biorxiv.org/content/10.1101/2023.05.31.542899v1.abstract',
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'name' => 'A neurodevelopmental epigenetic programme mediated bySMARCD3-DAB1-Reelin signalling is hijacked to promote medulloblastomametastasis.',
'authors' => 'Zou Han et al.',
'description' => '<p>How abnormal neurodevelopment relates to the tumour aggressiveness of medulloblastoma (MB), the most common type of embryonal tumour, remains elusive. Here we uncover a neurodevelopmental epigenomic programme that is hijacked to induce MB metastatic dissemination. Unsupervised analyses of integrated publicly available datasets with our newly generated data reveal that SMARCD3 (also known as BAF60C) regulates Disabled 1 (DAB1)-mediated Reelin signalling in Purkinje cell migration and MB metastasis by orchestrating cis-regulatory elements at the DAB1 locus. We further identify that a core set of transcription factors, enhancer of zeste homologue 2 (EZH2) and nuclear factor I X (NFIX), coordinates with the cis-regulatory elements at the SMARCD3 locus to form a chromatin hub to control SMARCD3 expression in the developing cerebellum and in metastatic MB. Increased SMARCD3 expression activates Reelin-DAB1-mediated Src kinase signalling, which results in a MB response to Src inhibition. These data deepen our understanding of how neurodevelopmental programming influences disease progression and provide a potential therapeutic option for patients with MB.</p>',
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<li>The tagmented libraries can then be purified using the MicroChIP DiaPure Columns (Cat. No. C03040001), and amplified.</li>
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<li>The tagmented libraries can then be purified using the MicroChIP DiaPure Columns (Cat. No. C03040001), and amplified.</li>
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<li>The tagmented libraries can then be purified using the MicroChIP DiaPure Columns (Cat. No. C03040001), and amplified.</li>
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$externalLink = ' <a href="https://doi.org/10.1073%2Fpnas" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118
×
