Cohesin ChIP-seq in multiple cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE206145 | GEO | 2022/06/17
REPOSITORIES: GEO
Similar Datasets
Project description:Cohesin is a protein complex that is essential for chromosome segregation. Cohesin regulates gene expression by insulation and chromatin domain formation with insulation factor CTCF. It was also reported that CTCF-independent cohesin-binding sites co-localize with transcription factors (TFs) for enhancer-promoter interaction. However, it is not a trivial task to assign whole-genome cohesin-binding regions into various functions. Also, the context-specific roles of cohesin-mediated interactions, especially on intragenic region, remains unsolved. To this end, we performed a comprehensive characterization of DNA-binding sites for cohesin and transcription factors (TFs) in MCF-7 cells with and without transcription stimulus. We integrated these epigenomic data with transcriptomic and chromatin interactions data to analyze context-specific cohesin function in genome-wide manner. As a result, we extracted a new subset of cohesin-binding sites named decreased intragenic cohesin sites (DICs), which were different from previous known functions of cohesin. DICs were negatively correlated with transcriptional regulation: a part of them were related to enhancer markers and “paused” RNA polymerase 2, while others contributed to chromatin architectures. The intron enriched DICs also showed chromatin de-compaction and special genomic bindings. Further conventional machine learning approach also captured similar DICs with distinguishable features. More importantly, DICs could be found in various tissues and cell lines, including cohesinopathy patient cells, to play a role in the disturbed transcription. These results suggested a novel function of cohesin on intragenic regions for gene transcription regulation.
2022-05-12 | GSE177045 | GEO
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Two-condition experiment, SA1 KO vs. WT cells. 3 Biological replicates.
2012-03-15 | E-GEOD-32234 | biostudies-arrayexpress
Project description:Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Cohesin binding pattern along some gene clusters is also affected by the lack of SA1, leading to dysregulation of the genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular etiology of CdLS. Examination of genome wide distribution of cohesin subunits in wildtype and SA1-null cells
2012-03-15 | E-GEOD-32319 | biostudies-arrayexpress
Project description:ChIP-seq profile of Spo13 binding sites arrested in prophase I by deletion of the meiotic transcription factor NDT80. Previous ChIP-ChIP data had indicated that Spo13 binding correlates with cohesin binding sites. Therefore, in addition to wild type cells, we also investigated cells deficient of the meiosis-specific cohesin subunit Rec8 to identify cohesin-dependent binding sites of Spo13.
2019-04-25 | GSE112170 | GEO
Project description:During cell division, transcription factors (TFs) are removed from chromatin twice, during DNA synthesis, and during condensation of chromosomes. How TFs can efficiently find their sites following these stages has been unclear. Here, we have analyzed the binding pattern of expressed TFs in human colorectal cancer cells. We find that binding of TFs is highly clustered, and that the clusters are enriched in binding motifs for several major TF classes. Strikingly, almost all clusters are formed around cohesin, and loss of cohesin decreases both DNA accessibility and binding of TFs to clusters. We show that cohesin remains bound in S phase, holding the nascent sister chromatids together at the TF cluster sites. Furthermore, cohesin remains bound to the cluster sites when TFs are evicted in early M-phase. These results suggest that cohesin binding functions as a cellular memory that promotes re- stablishment of TF clusters after DNA replication and chromatin condensation. Examination of TF binding by ChIP-seq in LoVo CRC cell-lines.
2013-08-15 | E-GEOD-49402 | biostudies-arrayexpress
Project description:During cell division, transcription factors (TFs) are removed from chromatin twice, during DNA synthesis, and during condensation of chromosomes. How TFs can efficiently find their sites following these stages has been unclear. Here, we have analyzed the binding pattern of expressed TFs in human colorectal cancer cells. We find that binding of TFs is highly clustered, and that the clusters are enriched in binding motifs for several major TF classes. Strikingly, almost all clusters are formed around cohesin, and loss of cohesin decreases both DNA accessibility and binding of TFs to clusters. We show that cohesin remains bound in S phase, holding the nascent sister chromatids together at the TF cluster sites. Furthermore, cohesin remains bound to the cluster sites when TFs are evicted in early M-phase. These results suggest that cohesin binding functions as a cellular memory that promotes re- stablishment of TF clusters after DNA replication and chromatin condensation. Examination of TF binding by ChIP-seq in a CRC cell-line.
2013-09-25 | E-GEOD-51142 | biostudies-arrayexpress
Project description:During cell division, transcription factors (TFs) are removed from chromatin twice, during DNA synthesis, and during condensation of chromosomes. How TFs can efficiently find their sites following these stages has been unclear. Here, we have analyzed the binding pattern of expressed TFs in human colorectal cancer cells. We find that binding of TFs is highly clustered, and that the clusters are enriched in binding motifs for several major TF classes. Strikingly, almost all clusters are formed around cohesin, and loss of cohesin decreases both DNA accessibility and binding of TFs to clusters. We show that cohesin remains bound in S phase, holding the nascent sister chromatids together at the TF cluster sites. Furthermore, cohesin remains bound to the cluster sites when TFs are evicted in early M-phase. These results suggest that cohesin binding functions as a cellular memory that promotes re- stablishment of TF clusters after DNA replication and chromatin condensation. Examination of TF binding by ChIP-seq in a CRC cell-line treated with non-targeting siRNA, or siRNA specific to the cohesin subunit RAD21.
2013-09-28 | E-GEOD-51234 | biostudies-arrayexpress
Project description:Chromosome segregation in mitosis and meiosis depends on sister chromatid cohesion mediated by cohesin complexes. Mutation of cohesin and other cohesion proteins causes transcriptional and developmental defects in animals and humans, but the molecular cause of these phenotypes is unknown. Here we describe 8811 cohesin binding sites in the human genome and show that the CCCTC-binding factor (CTCF) is associated with 88% of these. CTCF is dispensable for loading of cohesin onto DNA but is required for enrichment of cohesin at its binding sites. We provide evidence that cohesin is required for the role of CTCF sites in insulating promoters from distant enhancers. Like CTCF, cohesin is located on the maternal but not on the paternal allele of the H19 imprinting control region (ICR) and is required for imprinting of the H19-Igf2 locus. We find that cohesin is widely expressed in mammalian tissues, consistent with a cohesionindependent role in regulating gene expression. We propose that cohesin functions as a transcriptional insulator and speculate that subtle deficiencies in this function may be the cause of "cohesinopathies" such as Cornelia de Lange and Roberts syndrome. Keywords: ChIP-chip analysis
2008-01-30 | GSE9613 | GEO
Project description:During cell division, transcription factors (TFs) are removed from chromatin twice, during DNA synthesis, and during condensation of chromosomes. How TFs can efficiently find their sites following these stages has been unclear. Here, we have analyzed the binding pattern of expressed TFs in human colorectal cancer cells. We find that binding of TFs is highly clustered, and that the clusters are enriched in binding motifs for several major TF classes. Strikingly, almost all clusters are formed around cohesin, and loss of cohesin decreases both DNA accessibility and binding of TFs to clusters. We show that cohesin remains bound in S phase, holding the nascent sister chromatids together at the TF cluster sites. Furthermore, cohesin remains bound to the cluster sites when TFs are evicted in early M-phase. These results suggest that cohesin binding functions as a cellular memory that promotes re- stablishment of TF clusters after DNA replication and chromatin condensation. Examination of TF binding by ChIP-seq in a CRC cell-line treated with non-targeting siRNA, or siRNA specific to the cohesin subunit RAD21.
2013-10-01 | E-GEOD-51290 | biostudies-arrayexpress
Project description:ChIP-Seq targeting the major cohesin core subunit RAD21 to represent cohesin occupancy and binding sites in cohesin-mutated (STA2 or RAD21 mutations) and wildtpye adult AMLs.
| EGAD00001011199 | EGA