PRDM16 ChIP-Seq in Prdm16 WT and KO duodenal crypts
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ABSTRACT:
PROVIDER: PRJNA543833 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:PRDM16 ChIP was perfomed in control and Prdm16 KO crypts isolated from the duodenum of 6 week old mice 3 days after inducible gene deletion
2020-02-26 | GSE131487 | GEO
Project description:RNA-seq in Prdm16 KO duodenal crypts
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Project description:H3K27Ac ChIP-Seq in Prdm16 KO duodenal crypts
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Project description:The adult intestinal epithelium is maintained by a continuous replacement of differentiated cells from stem cells. Previous studies suggest that cellular metabolic pathways regulate intestinal stem cell activity and differentiation. However, little is known about the cell-intrinsic factors that control these metabolic programs. Here, we identify the transcription factor PRDM16 as a critical regulator of intestinal metabolic programing and stem cell differentiation. Acute deletion of Prdm16 in adult mice causes severe intestinal wasting, apoptosis, and an accumulation of poorly differentiated cells in the crypt. Prdm16-deficient crypts display decreased expression levels of fatty acid oxidation (FAO) genes and reduced rates of FAO. PRDM16 binds, along with its protein partners PPARγ and PPARα, to the promoter and enhancer regions of many FAO genes. The loss of Prdm16 or inhibition of FAO impaired the transition of intestinal stem cells into transit amplifying cells. Notably, PRDM16 expression is highest in the duodenum and declines distally along the intestine. This gradient of PRDM16 expression controls the region-specific expression of the FAO program and underlies the differential reliance of region-specific stem cells on FAO. Altogether, this study establishes PRDM16 as a regional-specific regulator of metabolism and stem cell differentiation in the intestine.
2020-02-26 | GSE121009 | GEO
Project description:The adult intestinal epithelium is maintained by a continuous replacement of differentiated cells from stem cells. Previous studies suggest that cellular metabolic pathways regulate intestinal stem cell activity and differentiation. However, little is known about the cell-intrinsic factors that control these metabolic programs. Here, we identify the transcription factor PRDM16 as a critical regulator of intestinal metabolic programing and stem cell differentiation. Acute deletion of Prdm16 in adult mice causes severe intestinal wasting, apoptosis, and an accumulation of poorly differentiated cells in the crypt. Prdm16-deficient crypts display decreased expression levels of fatty acid oxidation (FAO) genes and reduced rates of FAO. PRDM16 binds, along with its protein partners PPAR? and PPAR?, to the promoter and enhancer regions of many FAO genes. The loss of Prdm16 or inhibition of FAO impaired the transition of intestinal stem cells into transit amplifying cells. Notably, PRDM16 expression is highest in the duodenum and declines distally along the intestine. This gradient of PRDM16 expression controls the region-specific expression of the FAO program and underlies the differential reliance of region-specific stem cells on FAO. Altogether, this study establishes PRDM16 as a regional-specific regulator of metabolism and stem cell differentiation in the intestine.
2020-02-26 | GSE120897 | GEO
Project description:RNA was extracted from duodenal villi from crontrol and Prdm16 KO mice 3 days after deletion
2020-02-26 | GSE137888 | GEO
Project description:Group 1 -- WT or PRDM16-KO ex vivo murine MLL-AF9 cells, and PRDM16-KO AF9 cells overexpressing either f-PRDM16 or s-PRDM16. Group 2 -- WT or total PRDM16-KO murine HSCs isolated from adult BM. Group 3 -- WT or total PRDM16-KO murine HSCs isolated from fetal liver. Group 4 -- WT or f-PRDM16-KO murine HSCs (expressing s-PRDM16 only) isolated from fetal liver.
2018-06-08 | GSE112860 | GEO
Project description:As Prdm16 deficiency reduces self-renewal potential and depletes neural stem cells in culture we decided to investigate the underlying molecular mechanisms of the neural stem cells depletion in the Prdm16 deficient animals. For the experiment we used Prdm16Gt(OST67423)Lex (Prdm16LacZ) genetrap mice obtained from the NIH Mutant Mouse Regional Resource Center (http://www.mmrrc.org/). We compared the gene expression profiles of uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ (KO), Prdm16LacZ/+(HET), and Prdm16+/+ (WT) mice. The uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ, Prdm16LacZ/+, and Prdm16+/+ mice were dissected from the brains and placed into the Trizol reagent. Purified RNA was reverse transcribed and amplified using the WT-Ovation™ Applause WT/Amp RNA amplification system (NuGEN Technologies,) following the manufacturer’s instructions. Sense strand cDNA was fragmented and labeled using the FL-Ovation™ cDNA Biotin Module V2 (NuGEN). 2.5µg of labeled cDNA were hybridized to Affymetrix Mouse Gene ST 1.0 microarrays.
2010-09-09 | E-GEOD-23406 | biostudies-arrayexpress
Project description:As Prdm16 deficiency reduces self-renewal potential and depletes neural stem cells in culture we decided to investigate the underlying molecular mechanisms of the neural stem cells depletion in the Prdm16 deficient animals. For the experiment we used Prdm16Gt(OST67423)Lex (Prdm16LacZ) genetrap mice obtained from the NIH Mutant Mouse Regional Resource Center (http://www.mmrrc.org/). We compared the gene expression profiles of uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ (KO), Prdm16LacZ/+(HET), and Prdm16+/+ (WT) mice.
2010-09-09 | GSE23406 | GEO
Project description:We wanted to assess the role of a specific smooth muscle protein (MMP17) in two different intestinal compartments, the epithelium (crypts) and the smooth muscle. To do that we isolate intestinal crypts from wild-type (WT) and knockout (KO, Mmp17-/-) mice, and obtained clean strips of smooth muscle. After muscle dissociation, we obtained RNA directly from crypts and muscle, and it was used for RNA-seq. By comparing WT and KO samples we observed a higher impact in gene expression affecting crypts, even though MMP17 is only expressed in muscle. This helped us to identify altered signaling pathways in KO crypts that linked MMP17 with SMAD4 and BMP signaling.
2021-09-27 | E-MTAB-9180 | biostudies-arrayexpress