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The spliceosome factor sart3 regulates hematopoietic stem/progenitor cell development in zebrafish through the p53 pathway

ABSTRACT: The spliceosome factor sart3 regulates hematopoietic stem/progenitor cell development in zebrafish through the p53 pathway

PROVIDER: PRJNA756891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15564530_1.fastq.gz	Fastqsanger.gz
	SRR15564530_2.fastq.gz	Fastqsanger.gz
	SRR15564531_1.fastq.gz	Fastqsanger.gz
	SRR15564531_2.fastq.gz	Fastqsanger.gz
	SRR15564532_1.fastq.gz	Fastqsanger.gz

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The spliceosome factor sart3 regulates hematopoietic stem/progenitor cell development in zebrafish through the p53 pathway

Project description:Hematopoietic stem cells (HSCs) possess the potential for self-renew and the capacity, throughout life, to differentiate into all blood cell lineages. Yet, the mechanistic basis for HSC development remains largely unknown. In this study, we characterized a zebrafish smu471 mutant with hematopoietic stem/progenitor cell (HSPC) defects and found that sart3 was the causative gene. RNA expression profiling of the sart3smu471 mutant revealed spliceosome and p53 signaling pathway to be the most significantly enriched pathways in the sart3smu471 mutant. Knock down of p53 rescued HSPC development in the sart3smu471 mutant. Interestingly, the p53 inhibitor, mdm4, had undergone an alternative splicing event in the mutant. Restoration of mdm4 partially rescued HSPC deficiency. Thus, our data suggest that HSPC proliferation and maintenance require sart3 to ensure the correct splicing and expression of mdm4, so that the p53 pathway is properly inhibited to prevent definitive hematopoiesis failure. This study expands our knowledge of the regulatory mechanisms that impact HSPC development and sheds light on the mechanistic basis and potential therapeutic use of sart3 in spliceosome-mdm4-p53 related disorders.

2021-09-08 | GSE182560 | GEO

The spliceosome factor sart3 regulates hematopoietic stem/progenitor cell development in zebrafish through the p53 pathway.

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Ageing-associated proteome and acetylome of hematopoietic progenitor cells

Project description:Ageing-associated proteome and acetylome of hematopoietic progenitor cells

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Mutant p53 dysregulates gene transcription in hematopoietic stem and progenitor cells [RNA-seq 2]

Project description:We found that mutant p53 dysregulates gene transcription in hematopoietic stem and progenitor cells duirng aging.

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Mutant p53 dysregulates gene transcription in hematopoietic stem and progenitor cells [RNA-seq 1]

Project description:We found that p53 mutant hematopoietic stem and progenitor cells are resistant to iL-1ϐ treatment through altering inflammatory response.

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p53-mediated hematopoietic stem and progenitor cell competition

Project description:Cell competition was originally described in Drosophila as a process for selection of the fittest cells. Using genetic mosaic mouse models and bone marrow chimeras, we have characterized a form of cell competition that selects for the least damaged cells. This competition is controlled by p53 but is distinct from the classical p53-mediated DNA damage response: it persists for months, is specific to the hematopoietic stem and progenitor cells, and depends on the relative rather than absolute level of p53 in competing cells. The competition appears to be mediated by a non-cell autonomous induction of growth arrest and senescence-related gene expression in outcompeted cells with higher p53 activity. p53-mediated cell competition of this type could potentially contribute to the clonal expansion of incipient cancer cells. This microarray experiment is aimed at identification of candidate genes that mediate this competition. It compares mRNA expression patterns of HSCs with different levels of p53 activity in either competitive or non-competitive conditions (isolated from either wild type, mutant p53, or mosaic wt/mutant p53 mice (R26-mp53mice) after irradiation).

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p53-Dependent Induction of P2X7 on Hematopoietic Stem and Progenitor Cells Regulates Hematopoietic Response to Genotoxic Stress [RNA-seq]

Project description:Stem and progenitor cells are the main mediators of tissue renewal and repair, both under homeostatic conditions and in the response to physiological stress and injury. Hematopoietic system is responsible for the regeneration of blood and immune cells, and is maintained by bone marrow resident hematopoietic stem and progenitor cells (HSPCs). Hematopoietic system is particularly susceptible to injury in response to genotoxic stress, resulting in risk of bone marrow failure and secondary malignancies in cancer patients undergoing radiotherapy. Here we analyze the in vivo transcriptional response of HSPCs to genotoxic stress in a mouse whole body irradiation model, and together with p53 ChIP-Seq and studies in p53-knockout (p53KO) mice, characterize the p53-dependent and p53-independent branches of this transcriptional response. Our work demonstrates the p53-independent induction of inflammatory transcriptional signatures in HSPCs in response to genotoxic stress, and identifies multiple novel p53-target genes induced in HSPCs in response to whole body irradiation. In particular, we establish the direct p53-mediated induction of P2X7 expression on HSCs and HSPCs in response to genotoxic stress. We further demonstrate the role of P2X7 in hematopoietic response to acute genotoxic stress, with P2X7-deficiency significantly extending mouse survival in irradiation-induced hematopoietic failure. We also demonstrate the role of P2X7 in the context of long-term HSC regenerative fitness following sublethal irradiation. Overall our studies provide important insights into the mechanisms of HSC response to genotoxic stress and further suggests P2X7 as a target for pharmacological modulation of HSC fitness and hematopoietic response to genotoxic injury.

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