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Dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm

ABSTRACT: Dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm

PROVIDER: PRJNA578551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10315003.fastq.gz	Fastqsanger.gz
	SRR10315004.fastq.gz	Fastqsanger.gz
	SRR10315005.fastq.gz	Fastqsanger.gz
	SRR10315006.fastq.gz	Fastqsanger.gz
	SRR10315007.fastq.gz	Fastqsanger.gz

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Dominant role of DNA methylation over H3K9me3 in ERV silencing during embryonic endoderm development [ChIP-Dnmt]

Project description:Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications, such as H3K9me3 and DNA methylation. Their impact on ERV silencing differs in various cell types and, no systematic analyses on the interdependence between H3K9me3 and DNA methylation have been performed in differentiated cells. Here we show that deletion of the H3K9me3 HMTase Setdb1 in mouse embryonic endoderm results in ERV de-repression in only a subset of endoderm cells. We found that de-repression is restricted to visceral endoderm descendants and does not occur in definitive endoderm cells. Deletion of Setdb1 in visceral endoderm progenitors resulted in loss of H3K9me3 and reduced DNA methylation of IAPEz, consistent with up-regulation of this ERV family. In definitive endoderm cells, loss of Setdb1 did not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 ko resulted in ERV de-repression in both visceral and definitive endoderm cells, while H3K9me3 was unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 in ERV silencing in endoderm cells. Our findings suggest, that H3K9me3 is not sufficient for ERV silencing, but rather critical for maintaining high DNA methylation.

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Dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm.

Project description:Silencing of endogenous retroviruses (ERVs) is largely mediated by repressive chromatin modifications H3K9me3 and DNA methylation. On ERVs, these modifications are mainly deposited by the histone methyltransferase Setdb1 and by the maintenance DNA methyltransferase Dnmt1. Knock-out of either Setdb1 or Dnmt1 leads to ERV de-repression in various cell types. However, it is currently not known if H3K9me3 and DNA methylation depend on each other for ERV silencing. Here we show that conditional knock-out of Setdb1 in mouse embryonic endoderm results in ERV de-repression in visceral endoderm (VE) descendants and does not occur in definitive endoderm (DE). Deletion of Setdb1 in VE progenitors results in loss of H3K9me3 and reduced DNA methylation of Intracisternal A-particle (IAP) elements, consistent with up-regulation of this ERV family. In DE, loss of Setdb1 does not affect H3K9me3 nor DNA methylation, suggesting Setdb1-independent pathways for maintaining these modifications. Importantly, Dnmt1 knock-out results in IAP de-repression in both visceral and definitive endoderm cells, while H3K9me3 is unaltered. Thus, our data suggest a dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm cells. Our findings suggest that Setdb1-meditated H3K9me3 is not sufficient for IAP silencing, but rather critical for maintaining high DNA methylation.

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Dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm

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

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Dominant role of DNA methylation over H3K9me3 in ERV silencing during embryonic endoderm development [ChIP-Seq]

Project description:Dominant role of DNA methylation over H3K9me3 in ERV silencing during embryonic endoderm development [ChIP-Seq]

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