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

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

PROVIDER: PRJNA1088143 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28348713_1.fastq.gz	Fastqsanger.gz
	SRR28348713_2.fastq.gz	Fastqsanger.gz
	SRR28348714_1.fastq.gz	Fastqsanger.gz
	SRR28348714_2.fastq.gz	Fastqsanger.gz
	SRR28348715_1.fastq.gz	Fastqsanger.gz

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

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

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Mutant p53 dysregulates gene transcription in human CD34+ cells [RNA-seq 3]

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Mutant p53 alters chromatin accessibility in hematopoietic stem and progenitor cells.

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Mutant p53 dysregulates gene transcription in human CD34+ cells [RNA-seq 3]

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Mutant p53 alters chromatin accessibility in hematopoietic stem and progenitor cells [ATAC-seq]

Project description:Mutant p53 alters chromatin accessibility in hematopoietic stem and progenitor cells [ATAC-seq]

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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 [ChIP-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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