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Suppression of pervasive noncoding transcription in embryonic stem cells by esBAF

ABSTRACT: Approximately 75% of the human genome is transcribed, the majority of which does not encode protein. However, most noncoding RNA (ncRNA) is rapidly degraded after transcription, and relatively few have established functions, questioning the significance of this observation. Here we show that esBAF, a SWI/SNF family nucleosome remodeling factor, suppresses transcription of ncRNAs from approximately 57,000 nucleosome-depleted regions (NDRs) throughout the genome of mouse embryonic stem cells (ESCs). We show that esBAF functions both to keep NDRs nucleosome-free and to promote elevated nucleosome occupancy adjacent to NDRs. Reduction of adjacent nucleosome occupancy upon esBAF depletion is strongly correlated with ncRNA expression, suggesting that flanking nucleosomes form a barrier to pervasive transcription. Upon forcing nucleosome occupancy near an NDR using a nucleosome-positioning sequence, we find that esBAF is no longer required to silence transcription. These data reveal a novel role for esBAF in suppressing pervasive transcription from open chromatin regions in ESCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE57170 | GEO | 2015/02/12

SECONDARY ACCESSION(S): PRJNA245826

REPOSITORIES: GEO

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Suppression of pervasive noncoding transcription in embryonic stem cells by esBAF

Project description:Approximately 75% of the human genome is transcribed, the majority of which does not encode protein. However, most noncoding RNA (ncRNA) is rapidly degraded after transcription, and relatively few have established functions, questioning the significance of this observation. Here we show that esBAF, a SWI/SNF family nucleosome remodeling factor, suppresses transcription of ncRNAs from approximately 57,000 nucleosome-depleted regions (NDRs) throughout the genome of mouse embryonic stem cells (ESCs). We show that esBAF functions both to keep NDRs nucleosome-free and to promote elevated nucleosome occupancy adjacent to NDRs. Reduction of adjacent nucleosome occupancy upon esBAF depletion is strongly correlated with ncRNA expression, suggesting that flanking nucleosomes form a barrier to pervasive transcription. Upon forcing nucleosome occupancy near an NDR using a nucleosome-positioning sequence, we find that esBAF is no longer required to silence transcription. These data reveal a novel role for esBAF in suppressing pervasive transcription from open chromatin regions in ESCs. Examine nucleosome occupancy (MNase-Seq) and transcript production (CapSeq and RNA-Seq) in EGFP KD and Smarca4 KD ESCs

2015-02-12 | E-GEOD-57170 | biostudies-arrayexpress

BAF250a regulates nucleosome occupancy and histone modification in priming embryonic stem cell differentiation

Project description:BAF complex is one major group of chromatin remodeling factors in mammals. However, how BAF regulated nucleosomes and other histone modifications is not clear. Here we delete BAF250a, a major component in esBAF to study the nucleosome and histone changes in ESCs. We find that deletion of BAF250a leads to nucleosome occupancy increase in TSS regions and non-pioneer transcription factor binding sites. BAF250a deletion also cause overall decrease of H3K27me3 modification. Collectively, these results reveals how BAF complex coordinates nucleosome, histone modification to control ESC function. Sample 1-4: Nucleosome profiles in WT and BAF250a KO ESCs. Sample 5-10: profiling of H3K4me3 and H3K27me3 in WT and BAF250 KO ESCs.

2015-08-03 | E-GEOD-59082 | biostudies-arrayexpress

Regulation of nucleosome architecture and factor binding revealed by nuclease footprinting of the ESC genome

Project description:Functional interactions between gene regulatory factors and chromatin architecture have been difficult to directly assess. Here, we use micrococcal nuclease (MNase) footprinting to probe the functions of two chromatin remodeling complexes. By simultaneously quantifying alterations in small MNase footprints over the binding sites of 30 regulatory factors in mouse embryonic stem cells (ESCs), we provide evidence that esBAF and Mbd3/NuRD modulate the binding of several regulatory proteins. In addition, we find that nucleosome occupancy is reduced at specific loci in favor of subnucleosomes upon depletion of esBAF, including sites of histone H2A.Z localization. Consistent with these data, we demonstrate that esBAF is required for normal H2A.Z localization in ESCs, suggesting esBAF either stabilizes H2A.Z-containing nucleosomes or promotes subnucleosome to nucleosome conversion by facilitating H2A.Z deposition. Therefore, integrative examination of MNase footprints reveals insights into nucleosome dynamics and functional interactions between chromatin structure and key gene regulatory factors. Examine three read size footprints from MNase-Seq in EGFP KD, Mbd3 KD, and Smarca4 KD mESCs using ChIP-Seq datasets.

2015-08-27 | E-GEOD-68400 | biostudies-arrayexpress

Regulation of nucleosome architecture and factor binding revealed by nuclease footprinting of the ESC genome

2015-08-27 | GSE68400 | GEO

BAF250a regulates nucleosome occupancy and histone modification in priming embryonic stem cell differentiation

2015-08-03 | GSE59082 | GEO

Comparison of nucleosome occupancy and chromatin states between normal and cancer cell lines

Project description:Background: Epigenetic modification is a hallmark of cancer cells achieved through altered patterns of DNA methylation, histone modifications and nucleosome positions. These events have only been described in detail at gene promoters. Results: Here, we integrate multiple epigenome-wide maps to evaluate the scope of global epigenetic reprogramming in cancer cells at enhancers and insulators. Using high-resolution simultaneous mapping of global DNA methylation and nucleosome positions within individual DNA strands (NOMe-Seq), we observe a reorganization of the DNA methylome coupled with simultaneous modulation of nucleosome depleted regions (NDRs) at distal regulatory elements in cancer cells. We show that while NDRs are preferentially found at enhancers in normal breast and prostate epithelial cells, there are fewer NDRs coupled with increased DNA methylation detected at enhancersin cancer cells. Our data suggests that the acquisition of a nucleosome is key to DNA hypermethylation susceptibility and contributes to epigenetic silencing of enhancers in cancer, which can notably occur without loss of H3K4me1. Further we observe that NDRs are not necessary for peripheral phasing of adjacent nucleosomes, contrary to the common dogma, and show that nucleosomes remain organized and phased, even in the absence of a NDR as an anchor. Finally we observe the potential for transcription factors (TF) to organize NDRs genome-wide; all TF-binding sites are strongly hypomethylated and some show extensive peripheral nucleosome phasing. Conclusion: Together our findings suggest that, in addition to epigenetic alterations to promoter regions in cancer, there is substantial disruption to the distal regulatory architecture that provides an additional layer of epigenetic plasticity in malignancy. NOMe-seq, ChIP-seq for 5 marks and input control for breast normal (HMEC), breast cancer (MCF7), prostate normal (PrEC) and prostate cancer (PC3) cell lines

2014-06-04 | E-GEOD-57498 | biostudies-arrayexpress

Nucleosome organization dynamics during fertilization reveals regulation factors of zygotic gene activation in mouse (MNase-seq)

Project description:Chromatin remodeling is essential for epigenome reprogramming after fertilization. However, the underlying mechanisms of chromatin remodeling remain to be explored. Here, we investigated the dynamic changes in nucleosome occupancy and positioning in pronucleus-stage zygotes using low-input MNase-seq. We observed distinct features of inheritance and reconstruction of nucleosome position in both male and female genomes. Genome-wide de novo nucleosome occupancy in the paternal genome was observed as early as 1 hour after the injection of sperm. The nucleosome positioning pattern was continually rebuilt to form nucleosome depletion regions (NDRs) at promoters and transcription factor (TF) binding sites. NDRs formed more quickly on the promoters of genes involved in zygotic genome activation (ZGA), and their formation is closely connected with histone acetylation, but not transcription elongation or DNA replication. Importantly, we found that NDR establishment on the binding motifs of specific TFs might be associated with their potential pioneer functions in ZGA. Further investigations suggested that the predicted factors MLX and RFX1 played important roles in regulating minor and major ZGA, respectively. Our data not only elucidate the nucleosome positioning dynamics in both male and female pronuclei following fertilization, but also provide an efficient method for identifying key transcription regulators during development.

2022-04-02 | GSE140875 | GEO

Comparison of nucleosome occupancy and chromatin states between normal and cancer cell lines

2014-06-04 | GSE57498 | GEO

RSC and ISW1 Chromatin Remodelers Display Functional and Chromatin-based Promoter Antagonism [MNase-Seq]

Project description:ISWI-family chromatin remodelers organize nucleosome arrays, while SWI/SNF-family remodelers (RSC) disorganize and eject nucleosomes, implying an antagonism that is largely unexplored in vivo. Here, we describe two independent genetic screens for rsc suppressors that yielded mutations in the promoter-focused ISW1a complex, or mutations in the ‘basic patch’ of histone H4 (an epitope that regulates ISWI activity), strongly supporting RSC-ISW1a antagonism in vivo. RSC and ISW1a largely co-localize, and genomic nucleosome studies using rsc isw1 mutant combinations revealed opposing functions: promoters classified with a nucleosome-deficient region (NDR) gain nucleosome occupancy in rsc mutants, but this gain is attenuated in rsc isw1 double mutants. Furthermore, promoters lacking NDRs have the highest occupancy of both remodelers, consistent with regulation by nucleosome occupancy, and decreased transcription in rsc mutants. Taken together, we provide the first genetic and genomic evidence for RSC-ISW1a antagonism, and reveal different mechanisms at two different promoter architectures. Genome-wide nucleosome occupancy maps in RSC and rsc null strains were generated by paired-end sequencing of mononucleosomal DNA. Strains carrying the Sth1 degron allele and either pGal-UBR1 (YBC3386) or ubr1 null (YBC3387) represent RSC null and RSC wildtype, respectively.

2015-04-01 | E-GEOD-65593 | biostudies-arrayexpress

SWI/SNF and RSC cooperate to reposition and evict promoter nucleosomes at highly expressed genes in yeast

Project description:The nucleosome remodeling complex RSC functions throughout the yeast genome to set the positions of -1 and +1 nucleosomes and thereby determines the widths of nucleosome-depleted regions (NDRs). The related complex SWI/SNF participates in nucleosome remodeling/eviction and promoter activation at certain yeast genes, including those activated by transcription factor Gcn4, but does not appear to function broadly in establishing NDRs. By analyzing the large cohort of Gcn4-induced genes in mutants lacking the catalytic subunits of SWI/SNF or RSC, we uncovered cooperation between these remodelers in evicting nucleosomes from different locations in the promoter and in repositioning the +1 nucleosome downstream to produce wider NDRs, highly depleted of nucleosomes, during transcriptional activation. SWI/SNF also functions on par with RSC at the most highly transcribed constitutively expressed genes, suggesting general cooperation by these remodelers for maximal transcription. SWI/SNF and RSC occupancies are greatest at the most highly expressed genes, consistent with their cooperative functions in nucleosome remodeling and transcriptional activation. Thus, SWI/SNF acts comparably to RSC in forming wide, nucleosome-free NDRs to achieve high-level transcription, but only at the most highly expressed genes exhibiting the greatest SWI/SNF occupancies.

2018-03-23 | GSE110379 | GEO

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