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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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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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Tet and TDG Mediate DNA Demethylation Essential for MET in Somatic Cell Reprogramming

Project description:Tet-mediated DNA oxidation is a new type of epigenetic modification in mammals and its role in the regulation of cell fate transition remains poorly understood. Here, we derive mouse embryonic fibroblasts (MEFs) deleted in all three Tet genes and examine their capability to be reprogrammed into iPS cells. We demonstrate that these Tet-deficient MEFs cannot be reprogrammed due to a blockage in the mesenchymal-to-epithelial transition (MET). Reprogramming of MEFs deficient in TDG is similarly blocked. The blockage is caused by impaired activation of crucial microRNAs, which depends on oxidative demethylation promoted by Tet and TDG. Reintroduction of either miR-200c or catalytically active Tet and TDG restores reprogramming to the respective knockout MEFs. Thus, oxidative demethylation is essential for somatic cell reprogramming. These findings provide mechanistic insights into the operation of epigenetic barriers in cell lineage conversion. Reduced Representation Bisulfite (RRBS, MspI,~75-400bp size fraction) and Tet-Assisted RRBS (TARRBS) of MEFs & reprogramming MEFs at Day 5

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