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

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

PROVIDER: PRJNA1088141 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28348700_1.fastq.gz	Fastqsanger.gz
	SRR28348700_2.fastq.gz	Fastqsanger.gz
	SRR28348701_1.fastq.gz	Fastqsanger.gz
	SRR28348701_2.fastq.gz	Fastqsanger.gz
	SRR28348702_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 2]

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

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

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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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Ageing-associated proteome and acetylome of hematopoietic progenitor cells

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

2020-09-24 | PXD021651 |

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

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

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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

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