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An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells

ABSTRACT: An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells

PROVIDER: PRJNA291588 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2136760_1.fastq.gz	Fastqsanger.gz
	SRR2136760_2.fastq.gz	Fastqsanger.gz
	SRR2136770_1.fastq.gz	Fastqsanger.gz
	SRR2136770_2.fastq.gz	Fastqsanger.gz
	SRR2136761_1.fastq.gz	Fastqsanger.gz

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An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells (WGBS)

Project description:DNA methylation profoundly impacts genome regulation, notably through the control of transposons. DNA methylation is extensively remodeled during two developmental periods in mammals, gametogenesis and early embryogenesis. Most of transposons families become then hypomethylated, raising the question of their regulation in absence of DNA methylation. To induce genome-wide demethylation, we relied on hypomethylation-inducing culture conditions of murine embryonic stem cells. Surprisingly, we observed two phases of transposon regulation. After a burst of derepression, which correlates with DNA methylation disappearance, both LTR and non-LTR retrotransposons were efficiently re-silenced. While histone H3 lysine 9 trimethylation (H3K9me3) remained stable, H3 lysine 27 trimethylation (H3K27me3) was reorganized upon loss of DNA methylation and contributed to transposon re-silencing. Interestingly, we observed that H3K9me3 and H3K27me3 co-occurred but in distinct regions of unmethylated transposon sequences. This unusual pattern may provide a mechanistic relay ensuring genome stability during developmental periods of programmed loss of DNA methylation.

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An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells (RNA-Seq)

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An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells (ChIP-Seq)

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An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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An epigenetic switch ensures transposon repression upon dynamic loss of DNA methylation in embryonic stem cells.

Project description:DNA methylation is extensively remodeled during mammalian gametogenesis and embryogenesis. Most transposons become hypomethylated, raising the question of their regulation in the absence of DNA methylation. To reproduce a rapid and extensive demethylation, we subjected mouse ES cells to chemically defined hypomethylating culture conditions. Surprisingly, we observed two phases of transposon regulation. After an initial burst of de-repression, various transposon families were efficiently re-silenced. This was accompanied by a reconfiguration of the repressive chromatin landscape: while H3K9me3 was stable, H3K9me2 globally disappeared and H3K27me3 accumulated at transposons. Interestingly, we observed that H3K9me3 and H3K27me3 occupy different transposon families or different territories within the same family, defining three functional categories of adaptive chromatin responses to DNA methylation loss. Our work highlights that H3K9me3 and, most importantly, polycomb-mediated H3K27me3 chromatin pathways can secure the control of a large spectrum of transposons in periods of intense DNA methylation change, ensuring longstanding genome stability.

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Project description:An epigenetic switch ensures transposon repression upon acute loss of DNA methylation in ES cells (WGBS)

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