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STAT5 activation enhances Paneth cell function by regulated ileal Wnt3a-Tcf4-Sox9 or Gfi1 to sustain niche differentiation.

ABSTRACT: To determine the potential molecular mechanisms by which STAT5 signaling control ileal Paneth cell homeostasis, we isolated total RNA from ileal intact crypts of STAT5+/+, STAT5DIEC-/- and STAT5DIEC+++ mice and performed RNA sequencing (RNA-seq). With an average of 22.3 million reads per sample, we observed 27540 transcripts when reads were aligned to the mm10 genome with annotations provided by Ensembl. Transcripts were filtered, requiring at least 3 reads in 50% of samples within at least one condition, leaving 10197 transcripts for analysis. To identify differentially-regulated transcripts, we performed ANOVA (FDR-corrected p<0.05) and required the fold change to exceed 1.5.

ORGANISM(S): Mus musculus

PROVIDER: GSE112166 | GEO | 2019/03/21

REPOSITORIES: GEO

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STAT5 activation enhances Paneth cell function by regulated ileal Wnt3a-Tcf4-Sox9 or Gfi1 to sustain niche differentiation.

Project description:STAT5 activation enhances Paneth cell function by regulated ileal Wnt3a-Tcf4-Sox9 or Gfi1 to sustain niche differentiation.

| PRJNA442331 | ENA

To determine the potential molecular mechanisms by which STAT5 signaling controls colonic crypt homeostasis, we isolated total RNA from ileal intact crypts of STAT5+/+, STAT5DIEC-/- and STAT5DIEC+++ mice and performed RNA sequencing (RNA-seq).

Project description:Reads were aligned to the mm10 genome with annotations provided by Ensembl. Transcripts were filtered, requiring at least 3 reads in 50% of samples within at least one condition. To identify differentially-regulated transcripts, we performed ANOVA (FDR-corrected p<0.05) and required the fold change to exceed 1.5.

2019-04-02 | GSE112607 | GEO

Single cell RNA sequencing analysis of germ free (GF) mouse Paneth cells and microbiome-transferred exGF mouse Paneth cells.

Project description:The single cell level Paneth cell transcriptome under gnotobiotic condition has not been resolved. How gut microbiome modulates Paneth cell transcriptome at single cell level in germ-free mice was not known. We used a flow cytometry method to isolate highly pure ileal Paneth cells from germ free (GF) Paneth cell reporter mice (Lyz1-3'UTR-IRES-CreER) and from exGF Paneth cell reporter mice that were transplanted with wild type C57B/l6 mouse gut microbiota (exGF+B6M). These isolated Paneth cells were subjected to single cell RNA sequencing by 10xGenomics.

2023-09-01 | GSE237328 | GEO

Transcriptomic profile of intestinal epithelial cells obtained from ileal endoscopic biopsies from newly-diagnosed, pediatric Crohn's disease patients and healthy controls.

Project description:Purpose: To uncover differentially-regulated transcripts and pathways/biological processes in newly-diagnosed, pediatric Crohn's disease in comparison to healthy controls. Methods: Intestinal epithelial cells were dissociated from ileal endoscopic biopsies, and stored at -80C in RNAlater. The polyA RNA fraction was purified, and single-end, 50 bp reads were sequenced and aligned to the Hg19 genome using the TopHat2 aligner. Differential analysis was performed using Bioconductor packages including edgeR, where significance was defined as p<0.05 and fold change>2. Results: We obtained 15788 reasonably-expressed transcripts that were included in differential analyses. Conclusions: Our study characterizes the dysregulation of intestinal epithelial cells in treatment-naïve Crohn's disease using RNA sequencing for transcriptomic profile of cells obtained through ileal endoscopic biopsies.

2018-10-30 | GSE117875 | GEO

Mouse duodenal and ileal Paneth cell single cell RNA sequencing

Project description:An indepth analysis of Paneth cell transcriptome at single cell level has not been available. Existing intestinal epithelial cell scRNA dataset contain many cell types, where Paneth cells represent a small portion. We used a flow cytometry based approach to enrich and isolate relatively pure Panethc cells from a newly developed Paneth cell reporter mouse line (Lyz1-3'UTR-IRES-CreER; Rosa26R-tdTomato). Single cell RNA sequencing was performed on purified duodenal and ileal Paneth cells of mice housed under specific pathogen free condition.

2023-09-01 | GSE237327 | GEO

Tcf1 and Lef1 cooperate with CTCF and Stat5 to sustain CD8+ T cell homeostasis [ChIP-Seq]

Project description:An intricate interplay among Tcf1/Lef1, CTCF and Stat5 that orchestrates genomic architecture to coordinately promote CD8+ T cell homeostatic proliferation

2022-04-25 | GSE192758 | GEO

RNA-seq of Paneth cells

Project description:The impact of removal of Mll1 in intestinal Paneth cells expressing an constitutively active form of beta-catenin (beta-cateninGOF) was analysed in 4 pairs of sorted Paneth cells of Lgr5-CreERT2; beta-cateninGOF;Mll1+/- (control) and Lgr5-CreERT2; beta-cateninGOF;Mll1-/- (knockout) mice at 10 days after tamoxifen-induced mutagenesis. Using 75-base-pair reads, around 30 million reads per sample with comparable unique mapped reads (52-93%) were obtained. To analyze differentially expressed genes, we applied DESeq2 analysis to the RNA-seq dataset. Differentially expressed genes in beta-cateninGOF; Mll1-/- versus beta-cateninGOF; Mll1+/- Paneth cells showed both up- and downregulation of genes at a false discovery rate (FDR) of 10%. This included a global increase in the expression of goblet cell-specific genes. Downregulated genes included specific markers of Paneth cells, indicating that ablation of Mll1 in Paneth cells shifted their identity towards a mixed Paneth-goblet cell fate.

2022-01-08 | GSE177047 | GEO

Project description:Chip-seq of ileal intact crypts of STAT5+/+,STAT5DelN mice

| PRJNA748855 | ENA

Endothelial NO Synthase-Dependent S-Nitrosylation of β-Catenin Prevents Its Association with TCF4 and Inhibits Proliferation of Endothelial Cells Stimulated by Wnt3a.

Project description:Nitric oxide (NO) produced by endothelial NO synthase (eNOS) modulates many functions in endothelial cells. S-nitrosylation (SNO) of cysteine residues on β-catenin by eNOS-derived NO has been shown to influence intercellular contacts between endothelial cells. However, the implication of SNO in the regulation of β-catenin transcriptional activity is ill defined. Here, we report that NO inhibits the transcriptional activity of β-catenin and endothelial cell proliferation induced by activation of Wnt/β-catenin signaling. Interestingly, induction by Wnt3a of β-catenin target genes, such as the axin2 gene, is repressed in an eNOS-dependent manner by vascular endothelial growth factor (VEGF). We identified Cys466 of β-catenin as a target for SNO by eNOS-derived NO and as the critical residue for the repressive effects of NO on β-catenin transcriptional activity. Furthermore, we observed that Cys466 of β-catenin, located at the binding interface of the β-catenin-TCF4 transcriptional complex, is essential for disruption of this complex by NO. Importantly, Cys466 of β-catenin is necessary for the inhibitory effects of NO on Wnt3a-stimulated proliferation of endothelial cells. Thus, our data define the mechanism responsible for the repressive effects of NO on the transcriptional activity of β-catenin and link eNOS-derived NO to the modulation by VEGF of Wnt/β-catenin-induced endothelial cell proliferation.

| S-EPMC5452725 | biostudies-literature

Kinetochores read detyrosinated tubulin to sustain microtubule attachments

Project description:Post-translational cycles of α-tubulin detyrosination/tyrosination generate microtubule diversity, with broad physiological and clinical implications. However, the mechanistic understanding of how this microtubule diversity is decoded into specific cellular functions remains largely unknown. Here we show that the core microtubule-binding site at kinetochores ‘reads’ and responds to the α-tubulin detyrosination/tyrosination code. By combining CRISPR-Cas9 gene editing of enzymatic ‘writers’ of α-tubulin detyrosination/tyrosination in human cells, with biochemical purifications, mass spectrometry and super-resolution microscopy, we identified over a hundred proteins that preferentially associate with either detyrosinated or tyrosinated microtubules during mitosis. Among these, the conserved KNL-1/MIS12 complex/NDC80 complex (KMN) network at kinetochores showed a preference for tyrosinated microtubules. In addition to established roles in error correction and polar chromosome alignment, live-cell imaging uncovered a previously overlooked link between the α-tubulin detyrosination/tyrosination code and the formation of functional kinetochore-microtubule attachments, necessary for normal metaphase chromosome oscillations and timely spindle assembly checkpoint satisfaction. In vitro reconstitution experiments revealed that α-tubulin detyrosination specifically promotes Ndc80 diffusion along the microtubule lattice. We propose that the gradual accumulation of detyrosinated α-tubulin after initial microtubule capture at kinetochores facilitates the biased diffusion of core-binding proteins along the microtubule lattice, establishing a positive feedback loop that sustains kinetochore-microtubule attachments.

2024-10-03 | PXD047133 | Pride

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