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Genetic variation modulates aberrant DNA hypomethylation in naïve pluripotent stem cells.

ABSTRACT: Genetic variation modulates aberrant DNA hypomethylation in naïve pluripotent stem cells.

PROVIDER: PRJNA1110767 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29003548_1.fastq.gz	Fastqsanger.gz
	SRR29003548_2.fastq.gz	Fastqsanger.gz
	SRR29003549_1.fastq.gz	Fastqsanger.gz
	SRR29003549_2.fastq.gz	Fastqsanger.gz
	SRR29003550_1.fastq.gz	Fastqsanger.gz

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Genetic variation modulates aberrant DNA hypomethylation in naïve pluripotent stem cells

Project description:Genetic variation modulates aberrant DNA hypomethylation in naïve pluripotent stem cells

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Genetic variation modulates aberrant DNA hypomethylation in naïve pluripotent stem cells

Project description:Naïve pluripotent stem cells (nPSC) frequently undergo pathological and not readily reversible loss of DNA methylation marks at imprinted gene loci. This abnormality poses a hurdle for the use of pluripotent cell lines in biomedical applications and underscores the need to identify the causes underlying imprint instability in these cells. Here, we show that nPSCs from inbred mouse strains exhibit pronounced strain-specific susceptibility to locus-specific deregulation of imprinting marks during reprogramming to pluripotency and upon culture with MAP kinase inhibitors, the most common approach to maintain naïve pluripotency. Analysis of genetically highly diverse nPSCs from the Diversity Outbred (DO) stock confirms that genetic variation is a major determinant of epigenome stability in pluripotent cells. We leverage the variable DNA hypomethylation in DO lines to identify several trans-acting quantitative trait loci (QTLs) that determine epigenome stability at either specific target loci or genome-wide. Candidate factors encoded by two multi-target QTLs on chromosomes 4 and 17 suggest specific transcriptional regulators that contribute to methylation maintenance in nPSCs. We propose that genetic variants represent candidate biomarkers to identify pluripotent cell lines with desirable properties and might serve as entry points for the targeting engineering of nPSCs with stable epigenomes.

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Genetic variation modulates aberrant DNA hypomethylation in naïve pluripotent stem cells.

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CDCA7-associated global aberrant DNA hypomethylation translates to localized, tissue-specific transcriptional responses [RNA_seq_Spleen]

Project description:Disruption of Cell division cycle associated 7 (CDCA7) has been linked to aberrant DNA hypomethylation, but the impact of DNA methylation loss on transcription has not been investigated. Here, we show that CDCA7 is critical for maintaining global DNA methylation levels across multiple tissues in vivo. A pathogenic Cdca7 missense variant leads to the formation of large, aberrantly hypomethylated domains overlapping with the B genomic compartment but without affecting deposition of H3K9 trimethylation (H3K9me3). CDCA7-associated aberrant DNA hypomethylation translated to localized, tissue-specific transcriptional dysregulation that impacted large gene clusters. In brain, we identify CDCA7 as a transcriptional repressor and epigenetic regulator of clustered protocadherin isoform choice. Increased protocadherin isoform expression frequency is accompanied by DNA methylation loss, gain of H3K4 trimethylation (H3K4me3) and increased binding of the transcriptional regulator CCCTC-binding factor (CTCF). Overall, our in vivo work identifies a key role for CDCA7 in safeguarding tissue-specific expression of gene clusters via the DNA methylation pathway.

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