ChIP-seq for TCF7L2/TCF4 in E16.5 intestinal epithelial cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA690720 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13386926.fastq.gz | Fastqsanger.gz | |||
| SRR13386927.fastq.gz | Fastqsanger.gz |
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Project description:As part of our comprehensive characterization of intestinal development, we performed ChIP-seq for TCF7L2/TCF4 in mouse E16.5 intestinal epithelial cells. We identified more than 6000 regions bound by TCF7L2/TCF4 including a binding site in an enhancer driving Shh expression. Combined with transcriptional and functional analyses, our data reveal a novel cross-talk between WNT and Hedgehog signaling pathways.
2021-12-11 | GSE164442 | GEO
Project description:Most studies on TCF7L2 SNP variants in the pathogenesis of type 2 diabetes (T2D) focus on a role of the encoded transcription factor TCF4 in β-cells. Here, a mouse genetics approach shows that removal of TCF4 from β-cells does not affect their function, while manipulating TCF4 levels in the liver has major effects on metabolism. In Tcf7l2-/- mice, the immediate postnatal surge in liver metabolism does not occur. Consequently, pups die due to hypoglycemia. Combining chromatin immunoprecipitation with gene expression profiling, we identify a TCF4-controlled metabolic gene program that is acutely activated in the postnatal liver. In concordance, adult liver-specific Tcf7l2 knockout mice show reduced hepatic glucose production during fasting and display improved glucose homeostasis when maintained on high-fat diet. Furthermore, liver-specific TCF4 overexpression increases hepatic glucose production. These observations imply that TCF4 directly activates metabolic genes, and that inhibition of Wnt signaling may be beneficial in metabolic disease. RNA was extracted from liver tissues of the Tcf7l2 wildtype or knockout mice with treatments as indicated. Microarray analysis was performed to compare the expression profile changes between Tcf7l2 knockout and wildtype mice in response to treatment.
2012-11-01 | E-GEOD-41284 | biostudies-arrayexpress
Project description:Most studies on TCF7L2 SNP variants in the pathogenesis of type 2 diabetes (T2D) focus on a role of the encoded transcription factor TCF4 in β-cells. Here, a mouse genetics approach shows that removal of TCF4 from β-cells does not affect their function, while manipulating TCF4 levels in the liver has major effects on metabolism. In Tcf7l2-/- mice, the immediate postnatal surge in liver metabolism does not occur. Consequently, pups die due to hypoglycemia. Combining chromatin immunoprecipitation with gene expression profiling, we identify a TCF4-controlled metabolic gene program that is acutely activated in the postnatal liver. In concordance, adult liver-specific Tcf7l2 knockout mice show reduced hepatic glucose production during fasting and display improved glucose homeostasis when maintained on high-fat diet. Furthermore, liver-specific TCF4 overexpression increases hepatic glucose production. These observations imply that TCF4 directly activates metabolic genes, and that inhibition of Wnt signaling may be beneficial in metabolic disease.
2012-11-01 | GSE41284 | GEO
Project description:Genome-wide occupancy of Tcf7l2/Tcf4 in rat and expression profiling of Tcf7l2 mutant and control mice
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Project description:Surprisingly few pathways signal between cells, raising questions about mechanisms for tissue-specific responses. In particular, Wnt ligands signal in many mammalian tissues, including the intestinal epithelium, where constitutive signaling causes cancer. Genome-wide analysis of DNA cis-regulatory regions bound by the intestine-restricted transcription factor CDX2 in colonic cells uncovered highly significant over-representation of sequences that bind TCF4, a transcriptional effector of intestinal Wnt signaling. Chromatin immunoprecipitation confirmed TCF4 occupancy at most such sites and co-occupancy of CDX2 and TCF4 across short distances. A region spanning the single nucleotide polymorphism rs6983267, which lies within a MYC enhancer and confers colorectal cancer risk in humans, represented one of many co-occupied sites. Co-occupancy correlated with intestine-specific gene expression and CDX2 loss reduced TCF4 binding.These results implicate CDX2 in directing TCF4 binding in intestinal cells. Co-occupancy of regulatory regions by signal-effector and tissue-restricted transcription factors may represent a general mechanism for ubiquitous signaling pathways to achieve tissue-specific outcomes. A series of ChIP-chip experiments identified the CDX2 cistrome and discovered and validated extensive co-binding with TCF4 in colon cancer cell lines Transcriptional profiling following shRNA-mediated CDX2 knockdown was employed to identify CDX2-dependent gene expression in the human colon cancer cell line Caco2
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Project description:Analysis of the complex expression of claudin genes and transcription factors during intestinal epithelial cell differentiation across the crypt-to-surface colonic axis. Characterization of the complex expression gradients of transcription factors Hopx, Hnf4a, Klf4 and Tcfl2 and 12 claudin genes. In vitro confirmatory methods identified two pathways that stimulate claudin expression; Hopx/Klf4 activation of Cldn4, 7 and 15, and Tcf7l2/Hnf4a upregulation of Cldn23. Chromatin Immunoprecipitation confirmed a Tcf7l2/Hnf4a/Claudin23 cascade. Hnf4a conditional knockout mice fail to induce Cldn23 during colonocyte differentiation.
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Project description:Surprisingly few pathways signal between cells, raising questions about mechanisms for tissue-specific responses. In particular, Wnt ligands signal in many mammalian tissues, including the intestinal epithelium, where constitutive signaling causes cancer. Genome-wide analysis of DNA cis-regulatory regions bound by the intestine-restricted transcription factor CDX2 in colonic cells uncovered highly significant over-representation of sequences that bind TCF4, a transcriptional effector of intestinal Wnt signaling. Chromatin immunoprecipitation confirmed TCF4 occupancy at most such sites and co-occupancy of CDX2 and TCF4 across short distances. A region spanning the single nucleotide polymorphism rs6983267, which lies within a MYC enhancer and confers colorectal cancer risk in humans, represented one of many co-occupied sites. Co-occupancy correlated with intestine-specific gene expression and CDX2 loss reduced TCF4 binding.These results implicate CDX2 in directing TCF4 binding in intestinal cells. Co-occupancy of regulatory regions by signal-effector and tissue-restricted transcription factors may represent a general mechanism for ubiquitous signaling pathways to achieve tissue-specific outcomes.
2010-08-11 | GSE22572 | GEO
Project description:We performed genome-wide profiling of Tcf7l2 occupancy during oligodendrocyte differentiation and identified the key enzymes involved in cholesterol metabolism and essential for CNS myelination. Examination of Tcf7l2 chIP-seq in oligodendrocyte progenitor cell and 2 differentiation oligodendrocytes.
2016-02-19 | E-GEOD-65119 | biostudies-arrayexpress
Project description:Analysis of the complex expression of claudin genes and transcription factors during intestinal epithelial cell differentiation across the crypt-to-surface colonic axis. Characterization of the complex expression gradients of transcription factors Hopx, Hnf4a, Klf4 and Tcfl2 and 12 claudin genes. In vitro confirmatory methods identified two pathways that stimulate claudin expression; Hopx/Klf4 activation of Cldn4, 7 and 15, and Tcf7l2/Hnf4a upregulation of Cldn23. Chromatin Immunoprecipitation confirmed a Tcf7l2/Hnf4a/Claudin23 cascade. Hnf4a conditional knockout mice fail to induce Cldn23 during colonocyte differentiation. The distal colon tissue was obtained from 4 male, 10-12 week old, C57BL/6 (WT) mice. The Arcturus Laser Capture Microdissection (LCM) system (Applied Biosystems/Life Technologies) was used to isolate crypt-base and surface cell populations providing two samples per mouse (crypt-base and surface). This resulted in 8 total samples for microarray analysis.
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Project description:Primary intestinal epithelial cells were isolated from the proximal part of the small intestine from either E16.5 foetal tissue or adult tissue and embedded in matrigel for culturing in in advanced F12/DMEM supplemented with EGF, R-spondin and Noggin. RNA was extracted from cultures established from independent animals and subjected to expression profiling.
2017-11-30 | E-MTAB-5246 | biostudies-arrayexpress