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Stem cell niche ageing involves coordinated changes in transcription and alternative splicing

ABSTRACT: Stem cell niche ageing involves coordinated changes in transcription and alternative splicing

PROVIDER: PRJNA1189836 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31479083_1.fastq.gz	Fastqsanger.gz
	SRR31479083_2.fastq.gz	Fastqsanger.gz
	SRR31479084_1.fastq.gz	Fastqsanger.gz
	SRR31479084_2.fastq.gz	Fastqsanger.gz
	SRR31479085_1.fastq.gz	Fastqsanger.gz

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Stem cell niche ageing involves coordinated changes in transcription and alternative splicing

Project description:Gene expression (GE) determines the functionality and properties of cell types. Alternative splicing (AS) enhances the complexity of the transcriptome, expanding the protein interactome. As GE and AS jointly contribute to the formation of new interaction networks with potentially significant cellular functions, they could serve as the foundation for fundamental biological processes like ageing. Here, we investigate ageing in the Drosophila female germline stem cell (GSC) niche and describe functional changes in both GE and AS in aged flies. The GSC niche comprises escort cells, terminal filament cells and cap cells. Comparison of their transcriptomes reveals that, while all these cell types share genes exhibiting differential GE and AS variations related to cell adhesion, cytoskeleton and neural signalling during ageing, each population also experiences distinctive changes. This demonstrates unique ageing signatures within niche cell types. In addition and depending on the niche cell population, sets of genes display changes in both GE and AS, revealing a coordinated effort in the regulation of transcription and splicing during niche ageing. One such gene is Fasciclin 2, a neural adhesion molecule which we report to be essential for niche functioning. Furthermore, some genes involved in AS undergo changes in GE and/or AS themselves, providing a mechanistic explanation for the coordination of these two processes in the regulation of stem cell niche ageing. This is the case of the splicing factor Smu1, described here as a key element necessary for ovarian niche homeostasis.

2024-12-31 | GSE282708 | GEO

Drosophila ovarian stem cell niche ageing involves coordinated changes in transcription and alternative splicing.

Project description:Gene expression (GE) and alternative splicing (AS) contribute to the formation of new interaction networks with potentially significant cellular functions. Here, we investigate ageing in the Drosophila female germline stem cell (GSC) niche and describe functional changes in both GE and AS. The GSC niche comprises three types of support cells, whose ageing transcriptomes reveal differential GE and AS variations related to cell adhesion, cytoskeleton and neural signalling. Because each population show distinctive GE and AS changes, niche cell types possess unique ageing signatures. Depending on the cell population, groups of genes display changes in both GE and AS, revealing a coordinated regulation of transcription and splicing during niche ageing. One such gene is Fasciclin 2, a neural adhesion molecule that we find is essential for niche functioning. Furthermore, genes involved in AS undergo changes in GE and/or AS themselves, providing a mechanistic explanation for the coordination of these two processes during niche ageing. This is the case of the splicing factor Smu1, described here as a key element necessary for ovarian niche homeostasis.

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CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression

Project description:CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression

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SIRT7-induced PHF5A de-crotonylation regulates ageing progress through alternative splicing-mediated downregulation of CDK2

Project description:Dysregulation of protein post-translational modification (PTM) can lead to a variety of pathological process, such as abnormal sperm development, malignant tumorigenesis, depression, and ageing process. SIRT7 is a NAD + dependent protein deacetylase. Besides known deacetylation, SIRT7 may also have the capacity to remove other acylation. However, the roles of SIRT7-induced other de-acylation in ageing is still largely unknown. Here, we found that the expression of SIRT7 was significantly increased in senescent fibroblasts and aged tissues. Knockdown or overexpression of SIRT7 can inhibit or promote fibroblast senescence. Knockdown of SIRT7 led to increased pan- lysine crotonylation (Kcr) levels in senescent fibroblasts. Using modern mass spectrometry (MS) technology, we identified 5149 Kcr sites across 1541 protein in senescent fibroblasts, providing the largest crotonylome dataset to date in senescent cells. Specifically, among the identified protein, we found SIRT7 de-crotonylated PHF5A, an alternative splicing factor, at K25. De-crotonylation of PHF5A K25 contributed to decreased CDK2 expression by Retained Intron (RI) induced abnormal alternative splicing, thereby accelerating fibroblasts senescence, supporting a key role of PHF5A K25 de-crotonylation in ageing. Collectively, our data revealed the molecular mechanism of SIRT7-induced k25 decrotonylation of PHF5A regulating aging, and provide new ideas and molecular targets for drug intervention in cellular ageing and the treatment of aging-related diseases, indicating that protein crotonylation has important implication in the regulation of ageing progress.

2022-02-17 | PXD027232 | Pride

Axonogenesis is coordinated by alternative splicing programming and splicing regulator PTBP2

Project description:Axonogenesis is coordinated by alternative splicing programming and splicing regulator PTBP2

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CPEB3 regulates neuron-specific alternative splicing and involves neurogenesis gene expression [RNA-seq]

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Hematopoietic stem cells in perisinusoidal niches are protected from ageing [aged, GFP-label retaining HSCs]

Project description:With ageing, intrinsic hematopoietic stem cell (HSC) activity decreases, resulting in impaired tissue homeostasis, reduced engraftment following transplantation and increased susceptibility to diseases. However, whether ageing affects also the HSC niche impairing the capacity to support HSC function is still largely unknown. Here, by using in-vivo long-term label retention assays we demonstrate that aged labelling retaining (LR) HSCs, which are in the old mice the most quiescent HSC subpopulation with the highest regenerative capacity and cellular polarity, reside predominantly in perisinusoidal niches. Furthermore, we demonstrate that sinusoidal niches and perisinusoidal Nes-GFPlow cells are uniquely preserved in shape, morphology and number upon ageing. Finally, we show that myeloablative chemotherapy can selectively disrupt aged sinusoidal niches, which is linked to hematopoietic failure and decreased survival of aged mice. Overall, our data characterize for the first time the functional alterations of the aged HSC niche and unveil that perisinusoidal niches are uniquely preserved and protect HSCs from ageing.

2019-09-02 | GSE130298 | GEO

Axonogenesis is coordinated by alternative splicing programming and splicing regulator PTBP2

Project description:How a neuron acquires an axon is a fundamental question. Piecemeal identification of many axonogenesis-related genes has been done, but coordinated regulation is unknown. Through unbiased transcriptome profiling of immature primary cortical neurons during early axon formation, we discovered an association between axonogenesis and neuron-specific alternative splicing. Known axonogenesis genes exhibit little expression alternation but widespread splicing changes. Axonogenesis-associated splicing is governed by RNA binding protein PTBP2, which is enriched in neurons and peaks around axonogenesis in the brain. Cortical depletion of PTBP2 prematurely induces axonogenesis-associated splicing, causes imbalanced expression of axonogenesis-associated isoforms, and specifically affects axon formation in vitro and in vivo. PTBP2-controlled axongeneisis-associated Shtn1 splicing determines SHTN1’s capacity to regulate actin interaction, polymerization, and axon growth. Precocious Shtn1 isoform switch contributes to disorganized axon formation of Ptbp2-/- neurons. We conclude that PTBP2-orchestrated alternative splicing programming is required for robust generation of a single axon in mammals.

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Hematopoietic stem cells in perisinusoidal niches are protected from ageing [young and aged BM CD45-CD31+ endothelial cells]

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