Cohesin recruitment to promoters and enhancers by general transcription factors and chromatin regulators
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1196388 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR31667102_1.fastq.gz | Fastqsanger.gz | |||
| SRR31667102_2.fastq.gz | Fastqsanger.gz | |||
| SRR31667103_1.fastq.gz | Fastqsanger.gz | |||
| SRR31667103_2.fastq.gz | Fastqsanger.gz |
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Project description:Background Cohesin is a major regulator of three-dimensional genome organization and gene expression. Cohesin binds to DNA and dynamically extrudes a DNA loop, often bringing two cis-regulatory elements physically close together. Extruding cohesin molecules can be stalled or stabilized when they encounter a CTCF insulator protein on DNA, thereby anchoring a DNA loop. However, many enhancer-promoter loops that are bound by cohesin lack CTCF and it is not clear how cohesin is recruited to these sites in the genome. Results Here, we investigate the localization patterns of cohesin, as well as general chromatin state and localization of transcription factors WDR5, SP1, and NFYA in mouse embryonic stem cells. The SP1 and NFYA transcription factors are ubiquitously expressed proteins known to regulate expression of genes associated with a variety of cellular processes, while WDR5 is a core component of multiple complexes that regulate chromatin. Cohesin co-binds promoters and enhancers with WDR5, with SP1, or with NFYA in mESCs and other cell types. Cohesin co-immunoprecipitates with WDR5, SP1, and NFYA and cohesin simultaneously binds to the same chromatin molecules with these proteins. At co-bound sites, depletion of cohesin does not alter binding of WDR5, SP1, or NFYA;, however depletion of WDR5, SP1, or NFYA decreases cohesin binding. Conclusions These results indicate that general transcription factors and chromatin regulators recruit cohesin to specific sites in chromatin and thereby serve as structural regulators of enhancer-promoter loops via the recruitment of cohesin.
2025-06-09 | GSE283958 | GEO
Project description:The organisation of mammalian genomes into loops and topologically associated domains (TADs) regulates gene expression. The formation and maintenance of loops and TADs depends on the protein complex cohesin, which also holds replicated sister chromatids together from S phase until mitosis. To understand how cohesin functions, it is essential to know how many cohesin complexes and regulators exist in a typical cell and how they are distributed genome-wide. Here, we have used quantitative mass spectrometry, fluorescence-correlation spectroscopy and fluorescence recovery after photobleaching to measure the absolute number and dynamics of core subunits and regulators of the cohesin complex in human cells. We find that 60000 – 134000 cohesin complexes are bound to chromatin per G1 HeLa cell, suggesting that cohesin most likely does not occupy all its binding sites concurrently. We incorporate our data into mathematical models and discuss implications for how cohesin might contribute to genome organisation and sister chromatid cohesion.
2019-11-13 | PXD012712 | Pride
Project description:Recent works have shown that RNA Polymerase (Pol) II can be recruited to, and transcribe, distal regulatory regions. Here, we analyzed transcription initiation and elongation through genome-wide localization of Pol II, General Transcription Factors (GTFs) and active chromatin in developing T-cells. We show that Pol II and GTFs are recruited to known, highly T-cell-specific enhancers. We extend this observation for the first time to many new putative enhancers, a majority of which are transcribed with or without polyadenylation. Importantly, we also identify genomic features characterized by large Pol II/GTFs recruitment and Transcriptional Initiation Platforms (TIPs) at promoters, intergenic and intragenic regions. TIPs are characterized by variable widths (0.4 to 10 kb), and correlate with high CpG content and tissue-specificity at promoters. Finally, we also report differential recruitment of TFIID and other GTFs at promoters and enhancers. Overall, we propose that TIPs represent important novel regulatory hallmarks of the genome. This study is based on the analysis of 20 samples in mouse double-positive thymocytes, 15 of which cover a range of general and specific transcription factors, chromatin modifying enzymes as well as histone modifications. 2 samples were dedicated for strand-specific RNA sequencing either from the total RNA population or after a selection of Poly(A) RNA. A Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE) sample has been sequenced in order to isolate open chromatin regions. Finally, input and IG control samples were designed and sequenced for data processing purposes. Biological and technical replicates were processed as described in the supplementary methods.
2011-05-20 | E-GEOD-29362 | biostudies-arrayexpress
Project description:The CTCF paralog CTCFL disrupts cohesin at active promoters.
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Project description:Recent works have shown that RNA Polymerase (Pol) II can be recruited to, and transcribe, distal regulatory regions. Here, we analyzed transcription initiation and elongation through genome-wide localization of Pol II, General Transcription Factors (GTFs) and active chromatin in developing T-cells. We show that Pol II and GTFs are recruited to known, highly T-cell-specific enhancers. We extend this observation for the first time to many new putative enhancers, a majority of which are transcribed with or without polyadenylation. Importantly, we also identify genomic features characterized by large Pol II/GTFs recruitment and Transcriptional Initiation Platforms (TIPs) at promoters, intergenic and intragenic regions. TIPs are characterized by variable widths (0.4 to 10 kb), and correlate with high CpG content and tissue-specificity at promoters. Finally, we also report differential recruitment of TFIID and other GTFs at promoters and enhancers. Overall, we propose that TIPs represent important novel regulatory hallmarks of the genome.
2011-05-20 | GSE29362 | GEO
Project description:DNA G-quadruplexes contribute to CTCF and cohesin recruitment
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Project description:Sumoylation regulates general transcription factors at promoters of highly transcribed genes
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Project description:The enhancer regions of the myogenic master regulator MyoD give rise to at least two enhancer RNAs. CEeRNA regulates transcription of the adjacent MyoD gene while DRReRNA affects expression of Myogenin in trans. We found that DRReRNA is recruited at the Myogenin locus where it colocalizes with Myogenin nascent transcripts. DRReRNA associates with the Cohesin complex and such association correlates with its transactivating properties. Despite being expressed in undifferentiated cells, Cohesin is not loaded on Myogenin until the cells start expressing DRReRNA, which is then required for Cohesin chromatin recruitment and maintenance. Functionally, depletion of either Cohesin or DRReRNA reduces chromatin accessibility, prevents Myogenin activation, and hinders muscle cell differentiation. Thus, DRReRNA ensures spatially appropriate Cohesin loading in trans to regulate gene expression.
2018-06-01 | GSE113248 | GEO
Project description:We have measured absolute copy numbers and dynamics of cohesin, CTCF and their regulators NIPBL, WAPL and sororin by mass spectrometry, fluorescence-correlation spectroscopy and fluorescence recovery after photobleaching in HeLa cells before and after DNA replication. Comparison of these numbers with chromatin immunoprecipitation-sequencing data implies that some genomic cohesin and CTCF enrichment sites are unoccupied in single cells at any one time.
2019-11-21 | GSE126990 | GEO
Project description:It is currently assumed that 3D chromosomal organisation plays a central role in transcriptional control. However, recent evidence shows that steady-state transcription of only a minority of genes is affected by depletion of architectural proteins such as cohesin and CTCF. Here, we have used Capture Hi-C to interrogate the dynamics of chromosomal contacts of all human gene promoters upon rapid architectural protein degradation. We show that promoter contacts lost in these conditions tend to be long-range, with at least one interaction partner localising in the vicinity of topologically associated domain (TAD) boundaries. In contrast, many shorter-range chromosomal contacts, particularly those that connect active promoters with each other and with active enhancers remain unaffected by cohesin and CTCF depletion. We demonstrate that the effects of cohesin depletion on nascent transcription can be explained by changes in the connectivity of their enhancers. Jointly, these results provide a mechanistic explanation to the limited, but consistent effects of cohesin and CTCF on steady-state transcription and point towards the existence of alternative enhancer-promoter pairing mechanisms that are independent of these proteins.
2020-07-13 | GSE145735 | GEO