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H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE200976 | GEO | 2022/12/31

REPOSITORIES: GEO

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H3K27me3 Demethylases Maintain the Transcriptional and Epigenomic Landscape of the Intestinal Epithelium.

Project description:Background & aimsAlthough trimethylation of histone H3 lysine 27 (H3K27me3) by polycomb repressive complex 2 is required for intestinal function, the role of the antagonistic process-H3K27me3 demethylation-in the intestine remains unknown. The aim of this study was to determine the contribution of H3K27me3 demethylases to intestinal homeostasis.MethodsAn inducible mouse model was used to simultaneously ablate the 2 known H3K27me3 demethylases, lysine (K)-specific demethylase 6A (Kdm6a) and lysine (K)-specific demethylase 6B (Kdm6b), from the intestinal epithelium. Mice were analyzed at acute and prolonged time points after Kdm6a/b ablation. Cellular proliferation and differentiation were measured using immunohistochemistry, while RNA sequencing and chromatin immunoprecipitation followed by sequencing for H3K27me3 were used to identify gene expression and chromatin changes after Kdm6a/b loss. Intestinal epithelial renewal was evaluated using a radiation-induced injury model, while Paneth cell homeostasis was measured via immunohistochemistry, immunoblot, and transmission electron microscopy.ResultsWe did not detect any effect of Kdm6a/b ablation on intestinal cell proliferation or differentiation toward the secretory cell lineages. Acute and prolonged Kdm6a/b loss perturbed expression of gene signatures belonging to multiple cell lineages (adjusted P value < .05), and a set of 72 genes was identified as being down-regulated with an associated increase in H3K27me3 levels after Kdm6a/b ablation (false discovery rate, <0.05). After prolonged Kdm6a/b loss, dysregulation of the Paneth cell gene signature was associated with perturbed matrix metallopeptidase 7 localization (P < .0001) and expression.ConclusionsAlthough KDM6A/B does not regulate intestinal cell differentiation, both enzymes are required to support the full transcriptomic and epigenomic landscape of the intestinal epithelium and the expression of key Paneth cell genes.

| S-EPMC9971508 | biostudies-literature

H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium [CHIP-seq]

Project description:To determine the contribution of H3K27me3 demethylases to intestinal homeostasis, an inducible mouse model was used to simultaneously ablate Kdm6a and Kdm6b expression from the intestinal epithelium. We then performed RNA-Seq gene expression analysis at two timepoints (7 days and 5 months) following induction of Kdm6a and Kdm6b ablation. Differential H3K27me3 regions were also identified using ChIP-Seq at one time point (7 days) following gene ablation.

2022-12-31 | GSE200975 | GEO

H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium [RNA-seq]

2022-12-31 | GSE200974 | GEO

H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium.

Project description:H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium.

| PRJNA827792 | ENA

H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium [CHIP-seq]

Project description:H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium [CHIP-seq]

| PRJNA827795 | ENA

H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium [RNA-seq]

Project description:H3K27me3 demethylases maintain the transcriptional and epigenomic landscape of the intestinal epithelium [RNA-seq]

| PRJNA827796 | ENA

Transcriptomic and epigenomic profiling of H3K27me3 demethylases inhibitor GSK-J4 induced changes in colon cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-21 | GSE146679 | GEO

Inhibition of H3K27me3 Demethylases Promotes Plasmablast Formation.

Project description:B cell differentiation into Ab-secreting plasma cells requires transcriptional, metabolic, and epigenetic remodeling. Histone H3 lysine 27 trimethylation (H3K27me3), a histone modification associated with gene silencing, is dynamically regulated during B cell differentiation. Although several studies have focused on mechanisms involving the gain of this modification in plasmablasts (PB), the role of active demethylation of H3K27me3 by ubiquitously transcribed tetratricopeptide repeat, X chromosome (UTX) and Jumonji domain-containing protein 3 (JMDJ3) during B cell differentiation has not been examined. In this study, this process was assessed using a pharmacological inhibitor of UTX and JMJD3, GSK-J4. Treatment of ex vivo stimulated mouse B cells with GSK-J4 led to an increase in PB frequency without affecting the ability of the newly formed PB to secrete Abs. Consistent with the role of UTX and JMJD3 in promoting gene expression, the majority of differentially expressed were downregulated upon GSK-J4 treatment. GSK-J4-treated cells downregulated genes associated with signaling and P53 pathways. Inhibitor treated cells upregulated genes associated with cell cycle and proliferation, which correlated with an increase in actively proliferating cells. Unexpectedly, a majority of the downregulated transcripts corresponded to genes that in the wild-type setting were genes that gain H3K27me3 and downregulated in PB. Together, our results show that UTX and JMDJ3 are required to restrain B cell differentiation and suggest that they function as a rheostat for H3K27me3 to control this process.

| S-EPMC10197425 | biostudies-literature

CRWN nuclear lamina components maintain the H3K27me3 landscape and promote successful reproduction in Arabidopsis.

Project description:The nuclear lamina, a sub-nuclear protein matrix, maintains nuclear structure and genome function. Here, we investigate the role of Arabidopsis lamin analogs CROWDED NUCLEIs during gametophyte and seed development. We observed defects in crwn mutant seeds, including seed abortion and reduced germination rate. Quadruple crwn null genotypes were rarely transmitted through gametophytes. We focused on the crwn1 crwn2 (crwn1/2) endosperm, which exhibited enlarged chalazal cysts and increased expression of stress-related genes and the MADS-box transcription factor PHERES1 and its targets. Previously, it was shown that PHERES1 is regulated by H3K27me3 and that CRWN1 interacts with the PRC2 interactor PWO1. Thus, we tested whether crwn1/2 alters H3K27me3 patterns. We observed a mild loss of H3K27me3 at several hundred loci, which differed between endosperm and leaves. These data indicate that CRWNs are necessary to maintain the H3K27me3 landscape, with tissue-specific chromatin and transcriptional consequences.

| S-EPMC10592970 | biostudies-literature

Tankyrases maintain homeostasis of intestinal epithelium by preventing cell death.

Project description:Lgr5+ intestinal stem cells are crucial for fast homeostatic renewal of intestinal epithelium and Wnt/β-catenin signaling plays an essential role in this process by sustaining stem cell self-renewal. The poly(ADP-ribose) polymerases tankyrases (TNKSs) mediate protein poly-ADP-ribosylation and are involved in multiple cellular processes such as Wnt signaling regulation, mitotic progression and telomere maintenance. However, little is known about the physiological function of TNKSs in epithelium homeostasis regulation. Here, using Villin-creERT2;Tnks1-/-;Tnks2fl/fl (DKO) mice, we observed that loss of TNKSs causes a rapid decrease of Lgr5+ intestinal stem cells and magnified apoptosis in small intestinal crypts, leading to intestine degeneration and increased mouse mortality. Consistently, deletion of Tnks or blockage of TNKS activity with the inhibitor XAV939 significantly inhibits the growth of intestinal organoids. We further showed that the Wnt signaling agonist CHIR99021 sustains the growth of DKO organoids, and XAV939 does not cause growth retardation of Apc-/- organoids. Consistent with the promoting function of TNKSs in Wnt signaling, Wnt/β-catenin signaling is significantly decreased with stabilized Axin in DKO crypts. Together, our findings unravel the essential role of TNKSs-mediated protein parsylation in small intestinal homeostasis by modulating Wnt/β-catenin signaling.

| S-EPMC6177203 | biostudies-literature

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