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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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DOT1L-mediated H3K79 methylation in chromatin is dispensable for Wnt pathway-specific and other intestinal epithelial functions

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE41541: Expression data from mouse proximal intestinal epithelial Lgr5(hi) stem cells and differentiated villus cells (enterocytes from Atoh1 conditional knockout) GSE41542: H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells GSE41710: Global gene expression analysis of Dot1l-deficient and control intestinal villus cells in mouse Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Amit Sinha

PROVIDER: E-GEOD-41543 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Global gene expression analysis of Dot1l-deficient and control intestinal villus cells in mouse

Project description:Methylation of H3K79 is associated with chromatin at expressed genes, though it is unclear if this histone modification is required for transcription of all genes. Recent studies suggest that Wnt-responsive genes depend particularly on H3K79 methylation, which is catalyzed by the methyltransferase DOT1L. Human leukemias carrying MLL gene rearrangements show DOT1L-mediated H3K79 methylation and aberrant expression of leukemogenic genes. DOT1L inhibitors reverse these effects but their clinical use is potentially limited by toxicity in Wnt-dependent tissues such as intestinal epithelium. Genome-wide positioning of the H3K79me2 mark in Lgr5+ mouse intestinal stem cells and mature intestinal villus epithelium correlated with mRNA expression levels but not with Wnt-responsive genes per se. Selective Dot1l disruption in Lgr5+ stem cells or in all intestinal epithelial cells eliminated H3K79me2 from the respective compartments, allowing genetic evaluation of DOT1L requirements. Absence of methylated H3K79 did not impair health, intestinal homeostasis or expression of Wnt target genes in crypt epithelium for up to 4 months, despite increased crypt cell apoptosis. Global transcript profiles in Dot1l-null cells were barely altered. Thus, H3K79 methylation is not essential for transcription of Wnt-responsive or other intestinal genes and intestinal toxicity is not imperative when DOT1L is rendered inactive in vivo. Examination of differential gene expression between Dot1l control (Dot1 f/f) and Dot1l mutant (Villin-Cre, Dot1l f/f) villus cells.

2012-10-19 | E-GEOD-41710 | biostudies-arrayexpress

H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells

Project description:H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells Examination of H3K79me2 modifications between Lgr5(hi) stem cells and differentiated villus cells

2012-10-13 | E-GEOD-41542 | biostudies-arrayexpress

Expression data from mouse proximal intestinal epithelial Lgr5(hi) stem cells and differentiated villus cells (enterocytes from Atoh1 conditional knockout)

Project description:We used microarrays to detail the differentail gene expression between intestinal Lgr5(hi) stem cells and differentiated cells Assay the differential gene expression using total RNA from flow cytometry sorted Lgr5(hi) cells and EDTA isolated enterocytes from Atoh1 conditional knockout

2012-10-13 | E-GEOD-41541 | biostudies-arrayexpress

hMeDIP-seq of mouse intestinal stem and differentiated cells

Project description:We investigated genome-wide analysis of 5-hydroxymethylcytosine (5hmC) distribution in mouse intestinal stem and differentiated cells using hydroxyMethylated DNA immunoprecipitation (hMeDIP) followed by sequencing. Genomic DNA from mouse intestinal stem (Lgr5+) and villus differentiated cells were sonicated, immunoprecipitated by a 5hmC antibody, and sequenced in order to identify differential hydroxymethylated regions and genes.

2016-11-23 | E-MTAB-5202 | biostudies-arrayexpress

Gene expression in intestinal epithelial crypt and villus cell populations

Project description:We analyzed gene expression profiles in isolated mouse LGR5+ intestinal stem cells, lineage-specific enterocyte and secretory progenitors, and terminally differentiated villus enterocytes. Gene Ontology analyses of cell type-specific transcripts indicated their expected biological functions. We hybridized Affmetrix 430A 2.0 mouse microarrays with processed RNA isolated from purified Lgr5+ intestinal stem cells, secretory (Sec-Pro) and enterocyte (Ent-Pro) crypt progenitors, and mature villus enterocytes (ENT).

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RNA-seq of mouse Lgr5+ intestinal stem cells and progenitors following Lkb1 deletion against controls

Project description:Perturbed intestinal epithelial homeostasis demonstrated as decreased Lgr5+ intestinal stem cells (Lgr5 ISCs) and increased secretory lineages were observed in our study where Lkb1 was specfically deleted in Lgr5 ISCs using Lgr5-EGFP-creERT2 (Tamoxifen) deletor. To gain mechanistic insight how Lkb1 maintains intestinal epithelial stem cell homeostasis, Lkb1 deficient ISCs (Lgr5-high cells) and progenitors (Lgr5-low cells) are isolated by flow cytometry and profiled by RNA sequencing to compare with controls (Lkb1 wild type ISCs and progenitors).

2020-02-29 | E-MTAB-6501 | biostudies-arrayexpress

H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells

Project description:H3K79me2 ChIP-seq in mouse proximal intestinal Lgr5(hi) stem cells and villus cells

2012-10-13 | GSE41542 | GEO

Distinct processes and transcriptional targets underlie CDX2 requirements in intestinal stem cells and differentiated villus cells

Project description:To define target genes of the intestine-restricted transcription factor (TF) CDX2 in intestinal stem cells, we performed chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-Seq). We used RNA-sequencing to profile gene expression changes during cell differentiation from mouse intestinal stem cells to mature villus cells, as well as genes perturbed in intestinal stem cells upon loss of Cdx2. We find thousands of genes that change in expression during cell differentiation, including known stem cell and mature markers. Upon loss of Cdx2, hundreds of genes are up and down-regulated in intestinal stem cells, some of which are also bound by CDX2 nearby and constitute candidate direct target genes. CDX2 ChIP-Seq analysis of isolated mouse intestinal stem cells. RNA seq analysis of control mouse villus cells, control intestinal stem cells and Cdx2-deleted intestinal stem cells.

2015-09-15 | E-GEOD-70766 | biostudies-arrayexpress

Gene expression changes in Apc-mutant mouse intestinal organoids 7 and 20 days after the induction of the Apc deletion

Project description:We isolated and selected intestinal adenoma organoids from Lgr5-EGFP-IRES-CreER; Apcflox/flox mice and added tamoxifen to induce the deletion of the Apc gene in the intestinal stem cells. Gene expressions on day7 and day20 after the addition of tamoxifen were compared, representing two stages with different colorectal cancer stem cell content. Total RNA obtained from Lgr5-EGFP-IRES-CreER; Apcflox/flox organoids were compared 7 days and 20 days after the addition of tamoxifen, cultured without the Wnt-agonist R-Spondin1.

2015-12-31 | E-GEOD-47569 | biostudies-arrayexpress

Cdx2 transcription factor binding in intestinal villus and gene expression profiling in Cdx mutant mice

Project description:We conditionally inactivated mouse Cdx2, a dominant regulator of intestinal development, and mapped its genome occupancy in adult intestinal villi. Although homeotic transformation, observed in Cdx2-null embryos, was absent in mutant adults, gene expression and cell morphology were vitally compromised. Lethality was accelerated in mice lacking both Cdx2 and its homolog Cdx1, with exaggeration of defects in crypt cell replication and enterocyte differentiation. Cdx2 occupancy correlated with hundreds of transcripts that fell but not with equal numbers that rose with Cdx loss, indicating a predominantly activating role at intestinal cis-regulatory regions. Integrated consideration of a mutant phenotype and cistrome hence reveals the continued and distinct requirement in adults of a master developmental regulator that activates tissue-specific genes. Cdx2 ChIP-seq in mouse villus, and gene expression data from Cdx1, Cdx2 and compound knockout mouse intestine

2011-04-13 | E-GEOD-24633 | biostudies-arrayexpress

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