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FOXA and master transcription factors recruit Mediator and Cohesin to the core transcriptional regulatory circuitry of cancer cells

ABSTRACT: The Mediator and Cohesin complexes control the cellular transcriptional program. However, it is not well understood how they are recruited to regulatory regions. Our study shows that the core transcriptional regulatory circuitry of cancer cells is essential to recruit Mediator, Cohesin and NIPBL to enhancer and promoter regions of actively transcribed genes in cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76893 | GEO | 2016/10/24

SECONDARY ACCESSION(S): PRJNA308868

REPOSITORIES: GEO

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FOXA and master transcription factors recruit Mediator and Cohesin to the core transcriptional regulatory circuitry of cancer cells

Project description:The Mediator and Cohesin complexes control the cellular transcriptional program. However, it is not well understood how they are recruited to regulatory regions. Our study shows that the core transcriptional regulatory circuitry of cancer cells is essential to recruit Mediator, Cohesin and NIPBL to enhancer and promoter regions of actively transcribed genes in cancer cells. ChIP-seq analysis of Mediator (MED1), Cohesin (SMC1A) and NIPBL in HEPG2, A549 and MCF7 cells. The analysis also includes ChIP-Seq data for the transcription factor ERa in MCF7 cells treated with estradiol.

2016-10-24 | E-GEOD-76893 | biostudies-arrayexpress

FOXA and master transcription factors recruit Mediator and Cohesin to the core transcriptional regulatory circuitry of cancer cells.

Project description:Controlling the transcriptional program is essential to maintain the identity and the biological functions of a cell. The Mediator and Cohesin complexes have been established as central cofactors controlling the transcriptional program in normal cells. However, the distribution, recruitment and importance of these complexes in cancer cells have not been fully investigated. Here we show that FOXA and master transcription factors are part of the core transcriptional regulatory circuitry of cancer cells and are essential to recruit M ediator and Cohesin. Indeed, Mediator and Cohesin occupied the enhancer and promoter regions of actively transcribed genes and maintained the proliferation and colony forming potential. Through integration of publically available ChIP-Seq datasets, we predicted the core transcriptional regulatory circuitry of each cancer cell. Unexpectedly, for all cells investigated, the pioneer transcription factors FOXA1 and/or FOXA2 were identified in addition to cell-specific master transcription factors. Loss of both types of transcription factors phenocopied the loss of Mediator and Cohesin. Lastly, the master and pioneer transcription factors were essential to recruit Mediator and Cohesin to regulatory regions of actively transcribed genes. Our study proposes that maintenance of the cancer cell state is dependent on recruitment of Mediator and Cohesin through FOXA and master transcription factors.

| S-EPMC5064413 | biostudies-literature

Control of Embryonic Stem Cell State by Mediator and Cohesin (Agilent gene expression data)

Project description:The key transcription factors that control the embryonic stem cell gene expression program have been identified, but how they function to implement this program is not well understood. While screening for genes essential for maintenance of ES cell state, we identified many components of the Mediator and Cohesin complexes. Mediator and Cohesin were found to physically and functionally connect the enhancers and core promoters of active genes. An ES cell Mediator complex was found to copurify with Cohesin and its loading factor Nipbl, and normal levels of these proteins were essential for expression of the genes they occupy and for maintenance of ES cell state. See associated publication.

2010-08-12 | E-GEOD-22556 | biostudies-arrayexpress

Control of Embryonic Stem Cell State by Mediator and Cohesin (Illumina ChIP-Seq data)

2010-08-12 | E-GEOD-22562 | biostudies-arrayexpress

ChIP-Seq for NIPBL for SMC1 in human lymphoblastoid cells (hLCLs)

Project description:The gene expression program is regulated by a cell-type specific chromosome architecture. The connection between enhancer and promoter regions is dependent on a protein complex containing Nipbl, Mediator and Cohesin. To gain insights into the chromosome architecture of human differentiated cells, we profiled NIPBL and SMC1 in lymphoblastoid cells (LCLs). DNA was enriched from hLCLs and chromatin immunoprecipitations (ChIPs) were analyzed by Solexa sequencing. ChIPs were performed using an antibody against NIPBL and SMC1. Whole cell extract is provided for background.

2012-06-01 | E-GEOD-38395 | biostudies-arrayexpress

Control of Embryonic Stem Cell State by Mediator and Cohesin (Illumina ChIP-Seq data)

2010-08-12 | GSE22562 | GEO

Control of Embryonic Stem Cell State by Mediator and Cohesin (Agilent gene expression data)

2010-08-12 | GSE22556 | GEO

Transcription Factors Recruit the Cohesin Loader NIPBL to Promote Chromatin Looping and Long-range Gene Regulation

Project description:The cohesin complex is central to chromatin looping, but mechanisms by which these long-range chromatin interactions are formed and persist remain unclear. We demonstrate that interactions between a transcription factor and the cohesin loader NIPBL regulate enhancer-promoter looping and promote long-range gene regulation. Using mass-spectrometry, genome mapping, and single-molecule tracking methods, we demonstrate that NIPBL and cohesin regulate the dynamics and function of the glucocorticoid receptor (GR). Moreover, glucocorticoid treatment stabilizes NIPBL and cohesin interactions by promoting loop extrusion and chromatin looping. Patient-derived acute myeloid leukemia cells harboring cohesin mutations exhibit a reduced response to glucocorticoids (GCs), suggesting that the GR-NIPBL-cohesin interaction is defective in these patients, and they may be poor candidates for GC treatment.

2021-06-01 | GSE162617 | GEO

ChIP-Seq for NIPBL for SMC1 in human lymphoblastoid cells (hLCLs)

2012-06-01 | GSE38395 | GEO

A Mediator-cohesin axis controls heterochromatin domain formation

Project description:The genome consists of regions of transcriptionally active euchromatin and more silent heterochromatin. We reveal that the formation of heterochromatin domains requires cohesin turnover on DNA. Stabilization of cohesin on DNA through depletion of its release factor WAPL leads to a near-complete loss of heterochromatin domains. The Mediator CDK module controls heterochromatin in an opposing manner. Loss of this module leads to an almost binary partition of the genome into dense H3K9me3 domains, and regions devoid of H3K9me3 spanning the rest of the genome. By restricting the degree of heterochromatinization, the Mediator CDK module creates a transcription-permissive context that enables gene expression within heterochromatin domains. WAPL deficiency prevents the formation of heterochromatin domains, thus allowing for gene expression even in the absence of the Mediator CDK module. We propose that heterochromatin is controlled by two opposing activities, in which the Mediator CDK module and cohesin turnover must be balanced to enable the correct distribution of epigenetic marks to ensure proper gene expression.

2022-01-11 | GSE125631 | GEO

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