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.
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.
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.
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.
Project description:Ror gamma t-deficient mice lack group 3 Innate Lymphoid Cells (ILC3s) and as a result have increased tissue damage and diminished tissue repair in response to insult. To identify repair programs associated with ILC3 presence the transcriptomes of small intestinal stem cells exposed to damage in the presence or absence of ILC3 were compared. Small intestinal damage was induced in Ror gamma t-deficient Lgr5 reporter mice and littermate controls. Small intestinal epithelial stem cells were purified at days 1 and 4 after damage and subjected to RNA sequencing.
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).
Project description:We analyzed chromatin modifications, DNaseI-hypersensitive sites, and occupancy of a key secretory-lineage transcription factor, ATOH1. We found that lateral inhibition in the intestine occurs through ATOH1 exerting direct control within a broadly permissive chromatin state that is established in stem cells and is highly similar in specified progenitors of divergent potential. Mapping chromatin modifications (H3K4me2 and H3K27ac), DNaseI hypersensitivity (DHS), and ATOH1 binding sites in isolated intestinal crypt progenitors and mature intestinal 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.