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N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis [bulk RNA-seq]

ABSTRACT: The study explores the role of RNA methylation in the regulation of gut epithelial morphogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE181927 | GEO | 2021/09/30

REPOSITORIES: GEO

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N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis [scRNA-seq]

Project description:The study explores the role of RNA methylation in the regulation of gut epithelial morphogenesis.

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N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis

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

2021-09-30 | GSE181929 | GEO

N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis

Project description:N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis

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N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis [bulk RNA-seq]

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N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis [scRNA-seq]

Project description:N6-adenomethylation of GsdmC is essential for Lgr5+ stem cell survival and normal colon epithelial morphogenesis [scRNA-seq]

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N<sup>6</sup>-adenomethylation of GsdmC is essential for Lgr5<sup>+</sup> stem cell survival to maintain normal colonic epithelial morphogenesis.

Project description:Gut epithelial morphogenesis is maintained by intestinal stem cells. Here, we report that depletion of N6-adenosine methyltransferase subunit Mettl14 from gut epithelial cells in mice impaired colon mucosal morphogenesis, leading to increased mucosal permeability, severe inflammation, growth retardation, and premature death. Mettl14 ablation triggered apoptosis that depleted Lgr5+ stem cells and disrupted colonic organoid growth and differentiation, whereas the inhibition of apoptosis rescued Mettl14-deleted mice and organoids. Mettl14 depletion disrupted N6-adenomethylation on GsdmC transcripts and abolished GsdmC expression. Reconstitution of Mettl14-deleted organoids or mice with GSDMC rescued Lgr5 expression and prevented apoptosis and mouse premature death, whereas GSDMC silence eliminated LGR5 and triggered apoptosis in human colonic organoids and epithelial cells. Mechanistically, Mettl14 depletion eliminated mitochondrial GsdmC, disrupted mitochondrial membrane potential, and triggered cytochrome c release that activates the pro-apoptotic pathway. In conclusion, GsdmC N6-adenomethylation protects mitochondrial homeostasis and is essential for Lgr5+ cell survival to maintain normal colonic epithelial regeneration.

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Autophagy is essential for cardiac morphogenesis during vertebrate development

Project description:This study examined the effects of genetic knockdown of autophagy genes on vertebrate cardiac development We performed microarray studies comparing the hearts of control zebrafish embryos to the hearts of embryos with decreased expression of the autophagy genes atg5, becn1 or atg7. The results provide insight into the role of autophagy in developmental morphogenesis. Hearts were purified from 3 day-old zebrafish embryos injected with control or autophagy gene-specific morpholino oligonucleotides. RNA was prepared from all samples and hybridized to zebrafish-specific Affymetricx arrays.

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2024-04-01 | GSE230854 | GEO

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