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The transcription factor NF-Y participates in stem cell fate decision and regeneration in adult skeletal muscle

ABSTRACT: The transcription factor NF-Y participates in stem cell fate decision and regeneration in adult skeletal muscle

PROVIDER: PRJNA644871 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12172904_1.fastq.gz	Fastqsanger.gz
	SRR12172904_2.fastq.gz	Fastqsanger.gz
	SRR12172905_1.fastq.gz	Fastqsanger.gz
	SRR12172905_2.fastq.gz	Fastqsanger.gz
	SRR12172906_1.fastq.gz	Fastqsanger.gz

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The transcription factor NF-Y participates in stem cell fate decision and regeneration in adult skeletal muscle

Project description:The transcription factor NF-Y promotes cell proliferation and often loses its activity during differentiation through the regulation of NF-YA, the DNA binding subunit of the complex. In stem cell compartments, the shorter NF-YA splice variant (NF-YAs) is abundantly expressed and sustains their expansion. Here, we report that satellite cells, the stem cell population of adult skeletal muscle necessary for its growth and regeneration, express uniquely the longer NF-YA isoform (NF-YAl), majorly associated with cell differentiation. Through the generation of a conditional knock out mouse model that selectively ablates NF-YA in satellite cells, we demonstrate that NF-YA expression, and hence NF-Y activity, is fundamental to preserve the pool of muscle stem cells. Moreover, NF-Y supports their commitment to differentiation and ensures robust regenerative response to muscle injury. Gene expression profiling highlights an unexpected role for NF-Y in stem cell biology and opens a new scenario for NF-Y activity that is dispensable for muscle stem cell proliferation but required for efficient myogenic differentiation.

2021-08-30 | GSE154017 | GEO

The transcription factor NF-Y participates to stem cell fate decision and regeneration in adult skeletal muscle.

Project description:The transcription factor NF-Y promotes cell proliferation and its activity often declines during differentiation through the regulation of NF-YA, the DNA binding subunit of the complex. In stem cell compartments, the shorter NF-YA splice variant is abundantly expressed and sustains their expansion. Here, we report that satellite cells, the stem cell population of adult skeletal muscle necessary for its growth and regeneration, express uniquely the longer NF-YA isoform, majorly associated with cell differentiation. Through the generation of a conditional knock out mouse model that selectively deletes the NF-YA gene in satellite cells, we demonstrate that NF-YA expression is fundamental to preserve the pool of muscle stem cells and ensures robust regenerative response to muscle injury. In vivo and ex vivo, satellite cells that survive to NF-YA loss exit the quiescence and are rapidly committed to early differentiation, despite delayed in the progression towards later states. In vitro results demonstrate that NF-YA-depleted muscle stem cells accumulate DNA damage and cannot properly differentiate. These data highlight a new scenario in stem cell biology for NF-Y activity, which is required for efficient myogenic differentiation.

| S-EPMC8516959 | biostudies-literature

Telomere Shortening Impairs PGC Fate Decision

Project description:Telomere Shortening Impairs PGC Fate Decision

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Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

Project description:Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

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Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]

Project description:Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]

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Bcl6 mediates CD8+ T cell fate decision in cancer

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Stepwise cell fate decision pathways during osteoclastogenesis at single-cell resolution

Project description:To unveil cell fate decision pathways during osteoclast differentiation at single-cell resolution, we performed single-cell RNA sequencing (scRNA-seq) on the osteoclast culture system, in parallel with bulk RNA-seq and proteome analyses

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Pre-mRNA fate decision by TTP safeguards the fidelity of the inflammatory response

Project description:Successful immune responses are dependent on a precisely controlled balance between transcription and mRNA degradation. mRNA decay is driven through RNA-binding proteins (RBP), yet it remains unclear, how and when an individual mRNA molecule is selected for degradation. We investigated this fundamental question by using the anti-inflammatory RBP tristetraprolin (TTP, also known as Zfp36) as a model. Here, we show that TTP determines the fate of its targets concomitantly with their synthesis by binding to the pre-mRNA in the nucleus. Furthermore, we provide evidence that TTP orchestrates the target destabilization via a hierarchical molecular assembly that culminates by the association of mature mRNA with the RNA degradation machinery in the cytoplasm. The early fate decision in the life cycle of a TTP target mRNA prevents the translation of inflammatory mediators, particularly cytokine mRNAs, and promotes efficient cessation of the immune response. Importantly, the TTP homolog ZFP36L1 displays similar characteristics, suggesting a conserved mode of action within the ZFP36 family of RBPs.

2025-01-27 | PXD046381 | Pride

CRISPR screenings reveal neuropeptide orchestrate T helper cell fate decision

Project description:CRISPR screenings reveal neuropeptide orchestrate T helper cell fate decision

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