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Role of polycomb repressive complex 1 in the intestinal homeostasis [ChIP-Seq]

ABSTRACT: These data include the genome wide occupancy of histone modifications and transcription factors by ChIP sequencing in mouse crypt cells and in mouse ISCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE65318 | GEO | 2015/10/29

SECONDARY ACCESSION(S): PRJNA273665

REPOSITORIES: GEO

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Role of polycomb repressive complex 1 in the intestinal homeostasis [ChIP-Seq]

Project description:These data include the genome wide occupancy of histone modifications and transcription factors by ChIP sequencing in mouse crypt cells and in mouse ISCs. Immuno-precipitation of formaldehyde cross-linked chromatin prepared from wild type and Ring1a Ring1b dKO crypt cells and from WT ISCs using specific antibody against different target protein/modification.

2015-10-29 | E-GEOD-65318 | biostudies-arrayexpress

Role of polycomb repressive complex 1 in the intestinal homeostasis [ChIP-seq 2]

Project description:These data include the genome wide occupancy of histone modifications and transcription factors by ChIP sequencing in mouse villi cells and in mouse ISCs. Immuno-precipitation of formaldehyde cross-linked chromatin prepared from wild type Villi cells and wild type and Ring1a Ring1b dKO ISCs using specific antibody against different target protein/modification.

2015-10-29 | E-GEOD-71946 | biostudies-arrayexpress

Role of polycomb repressive complex 1 in the intestinal homeostasis [ChIP-seq 2]

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Role of polycomb repressive complex 1 in the intestinal homeostasis [RNA-Seq]

Project description:These data include RNA Seq data generated from wild type and Ring1a Ring1b dKO ISCs from Lgr5Gfp-CreERT2, Lgr5Gfp-CreERT2 Ring1a-/- Ring1bf/f, Lgr5Gfp-CreERT2-Ctnnb1-ex3 and Lgr5Gfp-CreERT2 Ring1a-/- Ring1bf/f-Ctnnb1-ex3 mice. Total RNA extracted from sorted wild type and Ring1a Ring1b dKO ISCs.

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Role of polycomb repressive complex 1 in the intestinal homeostasis [RNA-Seq]

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Polycomb Repressive Complex-2 (PRC2) regulates intestinal homeostasis.

Project description:Differential GRO-Seq and ChIP-Seq (H3K27me3) was performed on mouse mini-gut model cells.

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Role of polycomb repressive complex 1 in the intestinal homeostasis [RNA-seq 2]

Project description:These data include RNA Seq data generated from wild type and Ring1a Ring1b dKO Villi from Rosa26-CreERT2 Cdkn2a-/- and Rosa26-CreERT2 Cdkn2a-/- Ring1a-/- Ring1bf/f mice. Total RNA extracted from wild type and Ring1a Ring1b dKO Villi.

2015-10-29 | E-GEOD-71948 | biostudies-arrayexpress

Role of polycomb repressive complex 1 in the intestinal homeostasis [RNA-seq 2]

Project description:These data include RNA Seq data generated from wild type and Ring1a Ring1b dKO Villi from Rosa26-CreERT2 Cdkn2a-/- and Rosa26-CreERT2 Cdkn2a-/- Ring1a-/- Ring1bf/f mice.

2015-10-29 | GSE71948 | GEO

A constant pool of Lgr5+ intestinal stem cells is required for intestinal homeostasis

Project description:Lgr5+ crypt base columnar cells, the operational intestinal stem cells (ISCs), are thought to be dispensable for small intestinal (SI) homeostasis. Using a novel Lgr5-2A-DTR (Diphtheria Toxin Receptor) model which ablates Lgr5+ cells with near-complete efficiency and retains endogenous levels of Lgr5 expression, we show that persistent depletion of Lgr5+ ISCs in fact compromises SI epithelial integrity and reduces epithelial turnover in vivo. In vitro, Lgr5-2A-DTR SI organoids are unable to establish or survive when Lgr5+ ISCs are continuously eliminated when DT is in the media. However, transient exposure to DT at the start of culture allows organoids to form, and the rate of outgrowth reduces with increasing length of DT presence. Our results indicate that intestinal homeostasis requires a constant pool of Lgr5+ ISCs, which is supplied by rapidly reprogrammed non-Lgr5+ crypt populations when pre-existing Lgr5+ ISCs are ablated.

2020-12-31 | GSE148727 | GEO

PTEN-deficient intestinal stem cells initiate intestinal polyposis

Project description:Intestinal polyposis, a precancerous neoplasia, results primarily from an abnormal increase in the number of crypts. Crypts contain intestinal stem cells (ISCs). Thus intestinal polyposis provides an ideal condition for studying stem cell involvement in polyp/tumor formation. Using a conditional knock-out mouse model, we found that the tumor suppressor Phosphatase of Tension homolog (PTEN) governs the proliferation rate and number of ISCs and loss of PTEN results in an excess of ISCs. In PTEN mutants, excess ISCs initiate de-novo crypt formation and crypt fission, recapitulating crypt production in fetal/neonatal intestine. Microarray studies were used to profile the changes in gene expression that occurred when PTEN was knocked out in the intestine. Keywords: Disease state analysis, genetic modification, Intestinal polyposis, PTEN mutant, Cowden disease mouse model

2006-11-18 | GSE6078 | GEO

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