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.
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Project description:The T-cell factor 4 (Tcf4) protein (encoded by the Tcf7l2 gene) is a nuclear transcription regulator, which plays a key role in maintaining intestinal homeostasis, stem cell self-renewal and epithelial cell differentiation. Tcf4 has been identified as a crucial regulator of Paneth cell function in small intestinal crypts. It controls the expression of antimicrobial peptides and other effector molecules that contribute to the maintenance of the gut microbiota and protection against intestinal pathogens. The Defa6 promoter is active in adult Paneth cells and depletion of Tcf4 in these cells leads to loss of lysozyme production, altered morphology and mislocalization of these cells with the strongest phenotype in the ileum. To further investigate the function of Tcf4 in Paneth cells, we employed the Rosa26-tdTomato Tcf7l2-wt/wt Defa6-iCre mouse strain. In this strain, cells with an active Defa6 promoter are marked by expression of a red fluorescent protein (tdTomato). In parallel, heterozygous or homozygous deletion of the Tcf4 protein was obtained in Tcf7l2-flox/wt and Tcf7l2-flox/flox littermates, respectively. We performed gene expression profiling of Defa6-tdTomato+ cells from the distal part of the small intestine.
2026-05-01 | E-MTAB-13730 | biostudies-arrayexpress
Project description:The T-cell factor 4 (Tcf4) protein (encoded by the Tcf7l2 gene) is a nuclear transcription regulator, which plays a key role in maintaining intestinal homeostasis, stem cell self-renewal and epithelial cell differentiation. Tcf4 has been identified as a crucial regulator of Paneth cell function in small intestinal crypts. It controls the expression of antimicrobial peptides and other effector molecules that contribute to the maintenance of the gut microbiota and protection against intestinal pathogens. The Defa6 promoter is active in adult Paneth cells and depletion of Tcf4 in these cells leads to loss of lysozyme production, altered morphology and mislocalization of these cells with the strongest phenotype in the ileum. For deeper understanding of the Tcf4 function in the Paneth cell lineage, we employed the Rosa26-tdTomato Tcf7l2-wt/wt Defa6-iCre mouse strain. In this strain, cells with an active Defa6 promoter are marked by expression of a red fluorescent protein (tdTomato). In parallel, homozygous depletion of the Tcf4 protein was obtained in Tcf7l2-flox/flox littermates. We performed the single cell gene expression profiling of Defa6-tdTomato+ cells from the middle part of the small intestine.
2026-06-29 | E-MTAB-14489 | biostudies-arrayexpress
Project description:The transcription factor 4 (Tcf4) protein, which is encoded by the Tcf7l2 (transcription factor 7-like 2) gene, plays a key role in maintaining intestinal homeostasis, stem cell self-renewal and epithelial cell differentiation. Tcf4 has been identified as a key regulator of Paneth cell function in small intestinal crypts. It controls the expression of antimicrobial peptides and other effector molecules that contribute to the maintenance of the intestinal microbiota and protection against intestinal pathogens. Depletion of Tcf4 in mouse intestinal epithelial cells leads to loss of proliferating cells and dramatic changes in the morophology of the intestinal epithelum. To examine Tcf4 function in more detail, we used the Ki67-RFP Tcf7l2-flox/flox Villin-CreERT2 mouse strain. In this strain, proliferating cells are marked by expression of red fluorescent protein (RFP) and Tcf4 depletion from intestinal epithelial cells is accomplished by administration of tamoxifen. After 7 days, small red structures, i.e. \\"escaped crypts\\", appear in the epithelium, marking proliferative zones that appear to have escaped Tcf4 deletion. We performed gene expression profiling of RFP+ cells from these \\"escaped crypts\\" and from crypts isolated from wild-type epithelium.
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Project description:The T-cell factor 4 (Tcf4) protein (encoded by the Tcf7l2 gene) is a nuclear transcription regulator, which plays a key role in maintaining intestinal homeostasis, stem cell self-renewal and epithelial cell differentiation. Tcf4 has been identified as a key regulator of Paneth cell function in small intestinal crypts. It controls the expression of antimicrobial peptides and other effector molecules that contribute to the maintenance of the intestinal microbiota and protection against intestinal pathogens. Depletion of Tcf4 in mouse intestinal epithelial cells leads to loss of proliferating cells and dramatic changes in the morophology of the intestinal epithelum. To examine Tcf4 function in more detail, we used the Ki67-RFP Tcf7l2-flox/flox Villin-CreERT2 mouse strain. In this strain, proliferating cells are marked by expression of red fluorescent protein (RFP) and Tcf4 depletion from intestinal epithelial cells is accomplished by administration of tamoxifen. After 7 days, small red structures, i.e. \\"escaped crypts\\", appear in the epithelium, marking proliferative zones that appear to have escaped Tcf4 deletion. We performed gene expression profiling of RFP+ cells from these \\"escaped crypts\\" and from crypts isolated from wild-type epithelium.
2026-06-29 | E-MTAB-13731 | 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. 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:As part of our characterization of cellular complexity within our in vitro cultures, we performed scRNA-seq experiments analysing mouse E16.5 intestinal epithelial cells cultured 1) in conventional organoid cultures 3D or 2) as engineered tissues on microfabricated hydrogel scaffolds. We identified 6 transcriptionally disting clusters of both, fetal and adult identity highlighting the cellular complexity within our in vitro models.
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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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