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METTL3 modulates colonic epithelium integrity via maintaining the self-renewal and differentiation of Lgr5+ stem cell

ABSTRACT: METTL3 modulates colonic epithelium integrity via maintaining the self-renewal and differentiation of Lgr5+ stem cell

PROVIDER: PRJNA1017414 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26064458_1.fastq.gz	Fastqsanger.gz
	SRR26064458_2.fastq.gz	Fastqsanger.gz
	SRR26064459_1.fastq.gz	Fastqsanger.gz
	SRR26064459_2.fastq.gz	Fastqsanger.gz
	SRR26064460_1.fastq.gz	Fastqsanger.gz

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METTL3 modulates colonic epithelium integrity via maintaining the self-renewal and differentiation of Lgr5+ stem cell

Project description:We show that METTL3 expression is decreased in the colon mucosa in ulcerative colitis (UC) patients, and its expression is strongly associated with the differentiation and maturation of goblet cells during inflammation.Depletion of METTL3 significantly inhibits the self-renewal and differentiation of Lgr5+ stem cells, especially the differentiation and maturation of goblet cells, results in intestinal dysplasia and spontaneous inflammation.

2023-10-31 | GSE243214 | GEO

METTL3 modulates colonic epithelium integrity via maintaining the self-renewal and differentiation of Lgr5+ stem cell.

Project description: Not available

| S-EPMC12309382 | biostudies-literature

Small nucleolar RNA Snora61 drives self-renewal of small intestinal stem cells via initiation of Lgr5 transcription

Project description:Intestinal epithelium relies on intestinal stem cells (ISCs) for rapid and precise tissue replenishment to maintain gut normal function. The self-renewal maintenance of ISCs is finely regulated by multiple stemness factors and signaling pathways. However, the transcription mechanisms of some key stemness factors remain poorly understood. Here we identified that small nucleolar RNA Snora61 is highly expressed in ISCs. Snora61 is mainly distributed in the nucleoplasm. Snora61 knockout impairs ISC self-renewal and intestinal regeneration. Mechanistically, Snora61 binds to the promoter region of Lgr5 gene and engages with RNA-binding protein RBMX to recruit HMGB2 onto Lgr5 promoter, leading to Lgr5 transcription and expression. Snora61 promotes the self-renewal of small intestinal stem cells, which in turn enhances the proliferation of downstream differentiated cells, thereby contributing to the maintenance of intestinal homeostasis. Conversely, Snora61 knockout causes reduced LGR5 expression. Deletion of Lgr5 with Snora61 displays more severely impaired ISC self-renewal and intestinal regeneration. Our findings reveal a novel regulatory mechanism of Lgr5 transcription underlying ISC self-renewal maintenance.

2026-01-06 | GSE315692 | GEO

Lgr5-Expressing Chief Cells Drive Epithelial Regeneration and Cancer in the Oxyntic Stomach

Project description:Adult stem cells residing within tubular glands of the corpus epithelium are believed to fuel daily tissue renewal, but their identity remains controversial. Lgr5, marks both homeostatic stem cells and “reserve” stem cells in multiple tissues. Here, we report Lgr5 expression in a subpopulation of chief cells in mouse and human corpus glands. Using a new, non-variegated Lgr5-2A-CreERT2 mouse model, we show by cell fate mapping that Lgr5-expressing chief cells do not behave as corpus stem cells under homeostatic conditions, but are recruited to function as stem cells to effect epithelial renewal following injury. In vivo ablation of the Lgr5+ cells severely impairs epithelial homeostasis in the corpus, indicating an essential role in maintaining the resident stem cell pool. We additionally define the Lgr5+ chief cells as a major cell of origin of gastric metaplasia. These findings reveal clinically relevant insights into tissue homeostasis, repair and cancer in the corpus.

2017-05-01 | GSE86603 | GEO

Active Lgr5 Positive Stem Cells Drive Self-Renewal in the Pyloric Stomach and Efficiently Build Pyloric Units In-vitro

Project description:The Wnt target gene Lgr5 marks cycling stem cells in the small intestine, colon and hair-follicle. In the adult stomach, Lgr5 expression is confined to 3-4 proliferating cells at the gland base throughout the pylorus and limited numbers of corpus-type glands adjacent to the esophagus and squamous forestomach. In-vivo lineage tracing reveals that the pyloric Lgr5+ve cells rapidly generate all the major cell-types present in the gastric epithelium and maintain this multipotent stem cell activity over at least 20 months. In-vitro, single adult Lgr5+ve cells efficiently generate gastric units closely resembling mature pyloric glands. We conclude that Lgr5 is marking an active stem cell population at the base of the pyloric glands contributing to the long-term renewal of the adult gastric epithelium. The transcriptome of the adult Lgr5+ve stem cells harbors multiple Wnt target genes, implying a role for Wnt signaling in regulating pyloric stem cell function in-vivo. Conditional deletion of APC in these Lgr5+ve stem cells rapidly initiates tumor formation, supporting a potential role for aberrant Wnt signaling activity in gastric cancer.

2010-02-01 | GSE17485 | GEO

c-Kit+ cells that intercalate with crypt Lgr5+ cells are distinctively multipotent in colonic epithelium renewal and repair

Project description:c-Kit+ cells mark deep crypt secretory cells (DCSs) and supply Wnt3, EGF, and Notch signals to support their neighboring crypt bottom-intermingled Lgr5+ cells. We used single cells sequencing (scRNA-seq) to analyse the diversity and stemness of c-Kit+ cells in the colonic epithelium.

2025-03-25 | GSE259314 | GEO

METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

Altered cell lineage differentiation in fetal LGR5-null mice

Project description:The molecular mechanisms controlling stem cell renewal and lineage commitment are still poorly understood due to lack of reliable markers. In the adult small intestine, an example of high rate self-renewing tissue, four different epithelial cell lineages (enterocytes, Goblet, enteroendocrine and Paneth cells) are generated from a pool of stem cells localised at the bottom of the crypts of Lieberkühn. Recently, the orphan Leucine-rich repeat G protein-coupled receptor 5 (GPR49), a target of Wnt signalling, has been proposed as a marker for such cells. We investigated the role of LGR5 during intestinal development by using LGR5 null/LacZ-NeoR knock-in mice. We show that LGR5 deficiency leads to premature Paneth cell differentiation. X-gal staining on E18.5 intestine revealed that LGR5 expression is restricted to a few cells clustered within the intervillus region known to contain progenitor cells. In LGR5-null mice, expression from the LGR5 promoter was found upregulated, suggesting a loss of negative feedback control. However, neither epithelial cell proliferation nor cell migration appeared significantly impaired by LGR5 deficiency. Finally, transcriptional profiling of ileal mutant mice suggests that LGR5 plays a role in regulating the Wnt and Notch signalling pathways controlling progenitor renewal and differentiation.

2009-10-01 | GSE13337 | GEO

c-Kit+ cells that intercalate with crypt Lgr5+ cells are distinctively multipotent in colonic epithelium renewal and repair

Project description:c-Kit+ cells that intercalate with crypt Lgr5+ cells are distinctively multipotent in colonic epithelium renewal and repair

| PRJNA1080631 | ENA

METTL3 KD in HepG2 cells

Project description:To gain insight into possible processes that require m6A for their function, METTL3 was knocked down (KD) in HepG2 cells by siRNA transfections Differential expression analysis of METTL3 KD versus mock-transfected HepG2 cells, in 2 biological replicates

2012-04-25 | E-GEOD-37001 | biostudies-arrayexpress

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