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A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [Hi-C]

ABSTRACT: Purpose: Chromatin loop formation and maintenance is regulated by the cohesin complex. Here, we investigate whether a cancer mutation to a cohesin complex subunit, SMC1A-R586W, alters genome architecture. Method: Genome wide chromatin looping patterns were assessed via Hi-C in both wildtype and CRISPR-Cas9 genome edited SMC1A-R586W mouse embryonic stem cells (mESCs).

ORGANISM(S): Mus musculus

PROVIDER: GSE153574 | GEO | 2021/02/23

REPOSITORIES: GEO

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A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [RNA-seq]

Project description:Purpose: Chromatin loop formation and maintenance is regulated by the cohesin complex. Here, we investigate whether a cancer mutation to a cohesin complex subunit, SMC1A-R586W, alters genome architecture and gene expression. Method: Global gene expression was assessed using RNA-seq in wildtype and CRISPR-Cas9 genome edited SMC1A-R586W mouse embryonic stem cells (mESCs).

2021-02-23 | GSE153575 | GEO

A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [ChIP-seq]

Project description:Purpose: Chromatin loop formation and maintenance is regulated by the cohesin complex. Here, we investigate whether a cancer mutation to a cohesin complex subunit, SMC1A-R586W, alters genome architecture and gene expression. Method: Genome wide binding patterns of known architectural proteins and histone PTMs were assessed in WT and SMC1A-R586W mESCs by ChIP-seq.

2021-02-23 | GSE153573 | GEO

Regulation of Chromatin Looping by CTCF and Cohesin

Project description:As part of a study to understand the dynamics of chromatin looping and its regulation by CTCF and cohesin, we have determined the genome-wide binding profiles of CTCF and cohesin (Smc1a subunit) in a genome-edited mouse Embryonic Stem Cell (mESC) line referred to as clone C65. We have also performed 3D genome mapping using Micro-C in another genome-edited mESC line referred to as clone C36.

2021-12-31 | GSE187487 | GEO

The genomic landscape of cohesin-associated chromatin interactions

Project description:Cohesin is implicated in establishing tissue-specific DNA loops that target enhancers to promoters, and also localizes to sites bound by the insulator protein CTCF, which blocks enhancer-promoter communication. However, cohesin-associated interactions have not been characterized on a genome-wide scale. Here we performed chromatin interaction analysis with paired-end tag sequencing (ChIA-PET) of the cohesin subunit SMC1A in developing mouse limb. We identified 2,264 SMC1A interactions, of which 1,491 (65%) involved sites co-occupied by CTCF. SMC1A participates in tissue- specific enhancer-promoter interactions and interactions that demarcate regions of correlated regulatory output. In contrast to previous studies, we also identified interactions between promoters and distal sites that are maintained in multiple tissues, but are poised in embryonic stem cells and resolve to tissue-specific activated or repressed chromatin states in the mouse embryo. Our results reveal the diversity of cohesin- associated interactions in the genome and highlight their role in establishing the regulatory architecture of development. Smc1a ChIA-PET, RNA-seq, chromatin state maps (H3K27ac, H3K27me3, H3K4m2), and CTCF and Smc1a binding in mouse embryonic limb bud (E11.5)

2013-05-22 | E-GEOD-42237 | biostudies-arrayexpress

Cohesin profiling at DSBs

Project description:Chromatin undergoes major remodeling around DNA double strand breaks (DSB) to promote repair and DNA damage response (DDR) activation. We recently reported a high resolution map of gammaH2AX around multiple breaks on the human genome, using a new cell-based DSB inducible system. In an attempt to further characterize the chromatin landscape induced around DSBs, we now report the profile of SMC3, a subunit from the cohesin complex, previously characterized as required for repair by homologous recombination. We found that the recruitment of cohesin is moderate and restricted to the immediate vicinity of DSBs. In addition, we show that the cohesin complex, which was also recently proposed to be a key player in chromosome organisation and chromatin looping, controls gammaH2AX distribution within domains. Indeed, as we reported for transcription, cohesin binding antagonizes gammaH2AX spreading. Remarkably, depletion of cohesin leads to an increase of gammaH2AX at cohesin-bound genes (revelead by gammaH2AX mapping in upon SCC1 siRNA), associated with a decrease in their expression level after DSB induction. Thus our study identifies a novel role for the cohesin complex in protecting the genes located in gammaH2AX domains from both gammaH2AX spreading and transcriptional shut-down after DSB induction.

2012-01-01 | E-TABM-1164 | biostudies-arrayexpress

A WIZ/Cohesin/CTCF complex anchors DNA loops to define gene expression and cell identity [Hi-C]

Project description:Purpose: Chromatin architecture is an important regulator of gene expression, but details of how DNA loops form and function remain unclear. The purpose of this study is to assess the role of Widely Interspaced Zinc-fingers protein (WIZ) in gene regulation and DNA looping. Method: Genome wide chromatin looping patterns in the presence or absence of WIZ were assessed via Hi-C in both wildtype and CRISPR-Cas9 genome edited WIZ deletion mouse embryonic stem cells (mESCs).

2020-04-14 | GSE137274 | GEO

The genomic landscape of cohesin-associated chromatin interactions

2013-05-22 | GSE42237 | GEO

PDS5A and PDS5B differentially affect gene expression without altering cohesin localization across the genome [ChIP-seq]

Project description:Purpose: Cohesin is an important structural regulator of the genome. Whether cohesin HEAT repeat accessory proteins PDS5A and PDS5B differentially contribute to cohesin function remains unclear. The purpose of this study is to interrogate how PDS5A and PDS5B affect cohesin localization and gene expression in mouse embronic stem cells (mESCs) Method: Genome wide binding patterns of PDS5A, PDS5B, and cohesin in wildtype cells as well as in PDS5 CRISPR/Cas9 genome edited knockout cells were assessed via chromatin immunoprecipitation followed by high throughput sequencing (ChIP-seq). The redundancy of the PDS5 subunits was addressed by using siRNA against PDS5B in a PDS5A-knockout background.

2022-08-21 | GSE199354 | GEO

Distinct and overlapping roles of STAG1 and STAG2 in cohesin localization and gene expression in embryonic stem cells [RNA-seq]

Project description:Purpose: Cohesin is a ring-shaped complex that is critical to genome organization and is an important regulator of gene expression. How cohesin accessory proteins contribute to cohesin function remain unclear. The purpose of this study is to assess the roles of cohesin accessory proteins, STAG1 and STAG2, in cohesin localization and gene expression. Method: The role of STAG1 and STAG2 in gene regulation was assessed by performing RNA-seq in wildtype and CRISPR-Cas9 genome edited STAG knockout mouse embryonic stem cells (mESCs). The redundancy of the STAGs was addressed by using siRNA against STAG1 in a STAG2-knockout background.

2020-08-10 | GSE144115 | GEO

CRL4-DCAF15 control of cohesin dynamics sustains 1 cell proliferation

Project description:The CRL4-DCAF15 E3 ubiquitin ligase complex is targeted by the aryl-sulfonamide molecular glues, leading to neo-substrate recruitment, ubiquitination, and proteasomal degradation. However, the physiological function of DCAF15 remains unknown. Using a domain-focused genetic screening approach, we reveal DCAF15 as an acute myeloid leukemia (AML)-biased dependency. Loss of DCAF15 results in suppression of AML through compromised replication fork integrity and consequent accumulation of DNA damage. Accordingly, DCAF15 loss sensitizes AML to replication stress-inducing therapeutics. Mechanistically, we discover that DCAF15 directly interacts with the SMC1A protein of the cohesin complex and destabilizes the cohesin regulatory factors PDS5A and CDCA5. Loss of PDS5A and CDCA5 removal precludes cohesin acetylation on chromatin, resulting in uncontrolled chromatin loop extrusion, defective DNA replication, and apoptosis. Collectively, our findings uncover an endogenous, cell autonomous function of DCAF15 in sustaining AML proliferation through post-translational control of cohesin dynamics.

2023-08-19 | MSV000092697 | MassIVE

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