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Mus musculus

ABSTRACT: Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [RRBS]

OTHER RELATED OMICS DATASETS IN: E-GEOD-51786

PROVIDER: PRJNA227898 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1028850.fastq.gz	Fastqsanger.gz
	SRR1028851.fastq.gz	Fastqsanger.gz
	SRR1028852.fastq.gz	Fastqsanger.gz
	SRR1028843.fastq.gz	Fastqsanger.gz
	SRR1028853.fastq.gz	Fastqsanger.gz

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E-GEOD-51786

Project description:Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]

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Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation

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Project description:Reprogramming to iPSCs resets the epigenome of somatic cells including the reversal of X chromosome-inactivation. We sought to gain insight into the steps underlying the reprogramming process by examining the means by which reprogramming leads to X chromosome-reactivation (XCR). Analyzing single cells in situ, we found that hallmarks of the inactive X (Xi) change sequentially, providing a direct readout of reprogramming progression. Several epigenetic changes on the Xi occur in the inverse order of developmental X-inactivation, while others are uncoupled from this sequence. Among the latter, DNA methylation has an extraordinary long persistence on the Xi during reprogramming, and, like Xist expression, is erased only after pluripotency genes are activated. Mechanistically, XCR requires both DNA demethylation and Xist silencing, ensuring that only cells undergoing faithful reprogramming initiate XCR. Our study defines the epigenetic state of multiple sequential reprogramming intermediates and establishes a paradigm for studying cell fate transitions during reprogramming. RRBS profiles were generated from female and male ES cells, female iPS cells, SSEA1+ and SSEA1- reprogramming intermediates, and male and female MEFs, for a total of 18 samples.

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