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Genome-wide maps of Rad21 in R1/E embryonic stem cells and R1/E derived Embryoid bodies

ABSTRACT: ChIP-seq based determination of Rad21 binding sites in embryonic stem cells (ESC) and ESC derived Embryoid Bodies (EB) identified Examination of Rad21 binding sites in 2 cell types

ORGANISM(S): Mus musculus

SUBMITTER: Maciej Paszkowski-Rogacz

PROVIDER: E-GEOD-24029 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RAD21 cooperates with pluripotency transcription factors in the maintenance of embryonic stem cell identity.

Nitzsche Anja A Paszkowski-Rogacz Maciej M Matarese Filomena F Janssen-Megens Eva M EM Hubner Nina C NC Schulz Herbert H de Vries Ingrid I Ding Li L Huebner Norbert N Mann Matthias M Stunnenberg Hendrik G HG Buchholz Frank F

PloS one 20110512 5

For self-renewal, embryonic stem cells (ESCs) require the expression of specific transcription factors accompanied by a particular chromosome organization to maintain a balance between pluripotency and the capacity for rapid differentiation. However, how transcriptional regulation is linked to chromosome organization in ESCs is not well understood. Here we show that the cohesin component RAD21 exhibits a functional role in maintaining ESC identity through association with the pluripotency transc ...[more]

PMID: 21589869

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Genome-wide maps of CTCF in R1/E embryonic stem cells

Project description:ChIP-seq based determination of CTCF binding sites in embryonic stem cells (ESC) Examination of CTCF binding sites

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Genome-wide maps of Rad21 in R1/E embryonic stem cells and R1/E derived Embryoid bodies

Project description:ChIP-seq based determination of Rad21 binding sites in embryonic stem cells (ESC) and ESC derived Embryoid Bodies (EB) identified

2011-05-19 | GSE24029 | GEO

The Cohesin Complex Cooperates with Pluripotency Transcription Factors in the Maintenance of Embryonic Stem Cell Identity

Project description:Embryonic stem cells (ESCs) cells run a self-renewal gene expression program, requiring the expression of certain transcription factors accompanied by a particular chromosome organization to maintain a balance between pluripotency and the capacity for rapid differentiation. However, how transcriptional regulation is linked to chromosome organization in ESCs remains enigmatic. Here we show that Cohesin exhibits a functional role in maintaining ESC identity through association with the pluripotency transcriptional network. ChIP-seq analyses of the cohesin subunit Rad21 reveal an ESC specific cohesin binding pattern that is characterized by a CTCF independent colocalization of cohesin with pluripotency related transcription factors. Upon ESC differentiation, these binding sites disappear and instead new CTCF independent Rad21 binding sites emerge, which are enriched for binding sites of transcription factors implicated in early differentiation. Furthermore, knock-down of cohesin subunits causes expression changes that are reminiscent of the depletion of key pluripotency transcription factors, demonstrating the functional relevance of the cohesin - pluripotency transcriptional network association. Finally, we show that Nanog physically interacts with the cohesin interacting proteins Stag1 and Wapl, further substantiating this association. Based on these findings we propose that a dynamic placement of cohesin by pluripotency transcription factors contributes to a chromosome organization supporting the ESC expression program. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2011-05-19 | E-GEOD-24030 | biostudies-arrayexpress

Genome-wide mapping of Rad21 binding sites and gene expression profiling in wild type mouse small intestinal epithelial crypts and Apc Min adenomas

Project description:To investigate the role of RAD21 in the transcriptional regulation of global gene expression at early stage of colorectal cancer developments, we peformed the genome-wide analysis to map genomic regions bound by Rad21 in normal small testinal crypts and tumors (adenomas) harvested from Apc Min/+ mice using ChIP-seq. ChIP-seq naalysis identified high confidence RAD21 binding sites unique to normal crypts or adenomas, as well as those common to both tissues. We further performed RNA-seq to profile the changes in gene expression from normal WT crypts to adenomas at the very early stage of adenomagenesis in the context of Rad21 heterozygous loss. mRNA profiles of normal small intestinal crypts (WT) and adenomas from Apc Min/+ and Apc Min/+:Rad21+/- double mutant mouse; Mapping of Rad21 genomic binding sites in normal intestinal crypts (WT) and Apc Min/+ adenomas

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Rad21-mediated NF-κB signaling limits hematopoietic stem cell self-renewal in aging and inflammation

Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.

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Expression data from Rad21 knock-down in ES cells

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Expression data from RAD21 knockdown in MCF7 cells

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Expression data from RAD21 knockdown in MCF7 cells

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2016-06-01 | E-GEOD-82049 | biostudies-arrayexpress

Expression analysis of mock- or RAD21-transduced Kasumi1 cells

2013-07-16 | GSE47641 | GEO