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Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration

ABSTRACT: Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration

PROVIDER: PRJNA474910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7265530.fastq.gz	Fastqsanger.gz
	SRR7265540.fastq.gz	Fastqsanger.gz
	SRR7265550.fastq.gz	Fastqsanger.gz
	SRR7265560.fastq.gz	Fastqsanger.gz
	SRR7265570.fastq.gz	Fastqsanger.gz

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Similar Datasets

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration[intestine]

Project description:Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration[intestine]

| PRJNA474753 | ENA

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [colon]

Project description:Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [colon]

| PRJNA474734 | ENA

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration[intestine]

Project description:To define Atoh1 secretory signature, transcriptional profiling of secretory cells was performed. The expression profile of Atoh1+ cells from Atoh1(WT)CreERT2 R26RtdTom mice was determined by comparing tdTom+ (secretory) and tdTom- (absorptive) cells to define the baseline pro-secretory signature for small intestine (SI).

2018-08-06 | GSE115388 | GEO

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [colon]

2018-08-06 | GSE115378 | GEO

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [bulk RNA-seq]

Project description:Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [bulk RNA-seq]

| PRJNA474725 | ENA

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [bulk RNA-seq]

Project description:To compare secretory signatures of wildtype and mutant mice, the transcription profiles of tdTom+ cells from Atoh1(WT)CreERT2 R26RtdTom and Atoh1(9S/T-A)CreERT2 R26RtdTom mice were generated. The profiles were obtained for both small intestine (SI) and colon.

2018-08-06 | GSE115367 | GEO

Phospho-regulation of ATOH1 Is Required for Plasticity of Secretory Progenitors and Tissue Regeneration.

Project description:The intestinal epithelium is largely maintained by self-renewing stem cells but with apparently committed progenitors also contributing, particularly following tissue damage. However, the mechanism of, and requirement for, progenitor plasticity in mediating pathological response remain unknown. Here we show that phosphorylation of the transcription factor Atoh1 is required for both the contribution of secretory progenitors to the stem cell pool and for a robust regenerative response. As confirmed by lineage tracing, Atoh1+ cells (Atoh1(WT)CreERT2 mice) give rise to multilineage intestinal clones both in the steady state and after tissue damage. In a phosphomutant Atoh1(9S/T-A)CreERT2 line, preventing phosphorylation of ATOH1 protein acts to promote secretory differentiation and inhibit the contribution of progenitors to self-renewal. Following chemical colitis, Atoh1+ cells of Atoh1(9S/T-A)CreERT2 mice have reduced clonogenicity that affects overall regeneration. Progenitor plasticity maintains robust self-renewal in the intestinal epithelium, and the balance between stem and progenitor fate is directly coordinated by ATOH1 multisite phosphorylation.

| S-EPMC6138952 | biostudies-literature

Mediator Kinase Complexes Regulates ATOH1-Dependent Intestinal Differentiation

Project description:Cyclin Dependent Kinases CDK8 and CDK19 (Mediator kinase) are regulatory components of the Mediator complex, a highly conserved complex that fine tunes transcriptional output. While Mediator kinase has been implicated in the transcriptional control of key pathways necessary for development and growth, its function in vivo has not been well described. Herein, we report the consequences of complete ablation of both Cdk8/19 on tissue homeostasis. We show that intestinal epithelial specific deletion of Mediator kinase leads to a distinct defect in secretory progenitor differentiation with broad loss of the intestinal secretory cell types. Using a phospho-proteogenomic approach, we show that the Cdk8/19 kinase module interacts with and phosphorylates components of the chromatin remodeling complex Swi/Snf in intestinal epithelial cells. Genomic localisation of Swi/Snf and Mediator shows Cdk8/19-dependent genomic binding at distinct super-enhancer loci within key lineage specification genes, including the master regulator of secretory differentiation ATOH1. Using CRISPRi/CRISPRa, we identify a distinct Mediator- Swi/Snf bound enhancer element that is necessary and sufficient for ATOH1 expression in a Mediator-kinase dependent manner. As such, these studies uncover a newly described transcriptional mechanism of ATOH1-dependent intestinal cell specification that is dependent on the coordinated interaction of the chromatin remodeling complex Swi/Snf and Mediator complex.

2023-03-10 | PXD030212 | Pride

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration

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

2018-08-06 | GSE115416 | GEO

Intestinal secretory differentiation reflects niche-driven phenotypic and epigenetic plasticity of a common signal-responsive terminal cell [scRNA-Seq]

Project description:Enterocytes and four classic secretory cell types derive from intestinal epithelial stem cells. Based on morphology, location, and canonical markers, goblet and Paneth cells are considered distinct secretory types. Here, we report high overlap in their transcripts and sites of accessible chromatin, in marked contrast to those of their enteroendocrine or tuft cell siblings. Mouse and human goblet and Paneth cells express extraordinary fractions of few antimicrobial genes, which reflect specific responses to local niches. Wnt signaling retains some ATOH1+ secretory cells in crypt bottoms, where absence of BMP signaling potently induces Paneth features. Cells that migrate away from crypt bottoms encounter BMPs and thereby acquire goblet properties. These phenotypes and underlying accessible cis-elements interconvert in post-mitotic cells. Thus, goblet and Paneth properties represent alternative phenotypic manifestations of a common signal-responsive terminal cell type. These findings reveal exquisite niche-dependent cell plasticity and cis-regulatory dynamics in likely response to antimicrobial needs.

2025-04-08 | GSE271614 | GEO

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