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Asynchrony in the Exit from Naive Pluripotency (2024)

ABSTRACT: The asynchrony in the exit from naive pluripotency cannot be explained by differences in the cell cycle phase

PROVIDER: PRJEB74673 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR12865900.fastq.gz	Fastqsanger.gz
	ERR12865901.fastq.gz	Fastqsanger.gz
	ERR12865902.fastq.gz	Fastqsanger.gz
	ERR12865903.fastq.gz	Fastqsanger.gz

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Asynchrony in the Exit from Naive Pluripotency

Project description:The asynchrony in the exit from naive pluripotency cannot be explained by differences in the cell cycle phase

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Project description:Stem cells intrinsically express a subset of genes which are normally associated with interferon stimulation and the innate immune response. However, expression of these interferon stimulated genes (ISG) in stem cells is independent from external stimuli such as viral infection. Here, we show that the interferon regulatory factor 1, Irf1, is directly controlled by the murine formative pluripotency gene regulatory network and transiently upregulated during the transition from naive to formative pluripotency. IRF1 binds to regulatory regions of a conserved set of ISGs and is required for their faithful expression upon exit from naive pluripotency. We show that in the absence of IRF1, cells exiting the naive pluripotent stem cell state are more susceptible to viral infection. Irf1 therefore acts as a link between the formative pluripotency network, regulation of innate immunity genes and defense against viral infections during formative pluripotency.

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Transient upregulation of IRF1 during exit from naive pluripotency confers viral protection.

Project description:Stem cells intrinsically express a subset of genes which are normally associated with interferon stimulation and the innate immune response. However, the expression of these interferon-stimulated genes (ISG) in stem cells is independent from external stimuli such as viral infection. Here, we show that the interferon regulatory factor 1, Irf1, is directly controlled by the murine formative pluripotency gene regulatory network and transiently upregulated during the transition from naive to formative pluripotency. IRF1 binds to regulatory regions of a conserved set of ISGs and is required for their faithful expression upon exit from naive pluripotency. We show that in the absence of IRF1, cells exiting the naive pluripotent stem cell state are more susceptible to viral infection. Irf1 therefore acts as a link between the formative pluripotency network, regulation of innate immunity genes, and defense against viral infections during formative pluripotency.

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