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Homo sapiens

ABSTRACT: Assessing the impact of loss of ATF7IP and SETDB1 on the global distribution of H3K9me3

PROVIDER: PRJNA342602 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4237722.fastq.gz	Fastqsanger.gz
	SRR4237723.fastq.gz	Fastqsanger.gz
	SRR4237724.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:Assessing the impact of loss of MORC2 and SETDB1 on the global distribution of H3K9me3

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Project description:We find that HTT binds ATF7IP, a regulator of the histone H3 methyltransferase SETDB1. HTT inhibits the interaction of the ATF7IP-SETDB1 complex with other heterochromatin regulators and transcriptional repressors, maintaining low levels of H3K9 trimethylation (H3K9me3) in hESCs. Conversely, loss of HTT promotes global increased H3K9me3 levels. To test whether HTT knockdown also induces enrichment of H3K9me3 marks at specific genes, we performed chromatin immunoprecipitation (ChIP)-sequencing assays of hESCs using an antibody to H3K9me3.

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Assessing the impact of loss of ATF7IP and SETDB1 on the global distribution of H3K9me3

Project description:By comparing HeLa cells lacking ATF7IP or SETDB1 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of the SETDB1•ATF7IP complex on the distribution of the repress

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MGA directly recruits SETDB1/ATF7IP for histone H3K9me3 on meiosis-related genes in mouse embryonic stem cells.

Project description:Many of meiosis-related genes in mouse embryonic stem cells (ESCs) bear substantial amounts of trimethylated lysine 9 of histone H3 (H3K9me3) modification. However, how meiosis-related genes in ESCs acquire this histone modification is totally obscure. We hypothesize that the specific functional domain termed FAM of MGA that is the scaffolding component of PRC1.6, one of atypical subtypes of PRC1 is directly involved in the deposition of this histone modification by recruiting SETDB1 via its interaction with ATF7IP. To address the hypothesis, we generated ESCs producing MGA that lacks FAM domain and examined effects of the mutation on global expression profile and H3K9me3 levels by RNA- and ChIP-sequence analyses, respectively. We also generated ESCs producing mutant ATF7IP lacking its FNIII domain that is considered to be crucial for the interaction with MGA in our hypothesis to assess the role of the domain for the deposition of H3K9me3 by ChIP-seq analyses.

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Project description:Assessing the impact of loss of MORC2 on the transcriptome

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