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Genome-wide assessment of H4K20me1 chromatin profile in D458 shNull and shSETD8 medulloblastoma cells

ABSTRACT: Genome-wide assessment of H4K20me1 chromatin profile in D458 shNull and shSETD8 medulloblastoma cells

PROVIDER: PRJNA497788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8083534_1.fastq.gz	Fastqsanger.gz
	SRR8083534_2.fastq.gz	Fastqsanger.gz
	SRR8083535_1.fastq.gz	Fastqsanger.gz
	SRR8083535_2.fastq.gz	Fastqsanger.gz
	SRR8083536_1.fastq.gz	Fastqsanger.gz

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Genome-wide assessment of H4K20me1 chromatin profile in D458 shNull and shSETD8 medulloblastoma cells

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Project description:We compared the pattern of H4K20me1 at the L3 stage in wild-type and set-4 mutants by ChIP-seq. In wild-type, H4K20me1 levels on the X chromosome are higher than on autosomes. In set-4 mutants, this difference is lost. ChIP-seq of H4K20me1 at the L3 stage in wild-type and set-4 mutant L3 larvae.

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Project description:During X chromosome inactivation (XCI), in female mammals, gene silencing is initiated by a long-noncoding RNA, called Xist. Xist RNA accumulation also allows for the deposition of specific chromatin marks. Among others, PRC2-dependent H3K27me3 and PrSet7-dependent H4K20me1 become enriched at the inactive X chromosome. However, the dynamics of this process in relation to Xist RNA accumulation remains unknown as is the molecular mechanism allowing for H4K20me1 enrichment. To follow XCI dynamics in living cells, we developed a genetically encoded, H3K27me3-specific intracellular antibody, or H3K27me3-mintbody. By combining it with live-imaging of H4K20me1, the X chromosome and Xist RNA we uncover striking similarities in the accumulation dynamics of H3K27me3 and H4K20me1. Further ChIP-seq analysis confirmed concurrent accumulation of H4K20me1 and H3K27me3 during XCI albeit with distinct genomic distributions. Xist B and C repeat mutant, which can silence the X but does not allow for H3K27me3 enrichment, also showed lack of H4K20me1 deposition. Thus, both H3K27me3 and H4K20me1 are deposited at the inactive X through a common molecular mechanism but are dispensable for the initiation of gene silencing.

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