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ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 binding capacity at PBS-Lys elements.

ABSTRACT: ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 binding capacity at PBS-Lys elements.

PROVIDER: PRJNA658492 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12491254_1.fastq.gz	Fastqsanger.gz
	SRR12491254_2.fastq.gz	Fastqsanger.gz
	SRR12491255_1.fastq.gz	Fastqsanger.gz
	SRR12491255_2.fastq.gz	Fastqsanger.gz
	SRR12491256_1.fastq.gz	Fastqsanger.gz

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ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 binding capacity at PBS-Lys elements.

Project description:We performed ChIP-seq assay with anti-GFP antibodies on Zfp961-GFPflox/flox ESCs.We found PBS-Lys-containing endogenous virus K subgroup repeats (ERV-K) were significantly enriched in the strong peak regions (40%, 165 out of 413), compared to their abundance in the mouse genome (~5%), suggesting Zfp961 binding preference towards ERV-K regions. And Zfp961 has a PBS-Lys motif. We performed H3K9me3 ChIP on Zfp961 WT or KO mESCs. We found that Zfp961 recruits H3k9me3 modification at ERVKs, and H3K9me3 level showed a moderate decrease upon Zfp961 deletion.

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ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 repression capacity to transcription of ERVKs

Project description:We performed ChIP-seq assay with anti-KAP1 antibodies on Zfp961-GFPflox/flox ESCs.We found KAP1 signal decreased at PBS-Lys sites in Zfp961 KO cells compared to WT, suggesting Zfp961 recruiting KAP1 to ERV-K regions. We performed H3K27ac ChIP on Zfp961 WT or KO mESCs. We found that H3k27ac modification at PBS-Lys sites was elevated upon Zfp961 deletion, indicating Zfp961 serving as a repressive transcription factor.

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ChIP-seq on Znf417 and Znf587 overexpression 293T to verify Znf417 and Znf587 binding capacity at PBS-Lys elements.

Project description:The ChIP-seq experiments using GFP antibody on ZNF417/ZNF587-GFP overexpressing 293T cells revealed that ZNF417/ZNF587 preferred to bind a PBS-Lys-containing HERVs. Further motif calling analysis showed that both ZNF417 and ZNF587 bind to HERVK PBS-resembled motif.

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RNA-seq on Zfp961 GFP flox/flox mESCs to verify ERVKs repression by Zfp961.

Project description:To investigate the functional consequences in the absence of ZFP961 in mESCs, we treated the Zfp961-GFPflox/flox cells with 4-OHT to deplete the ZFP961 alleles, and then performed RNA-seq on three independent Zfp961-GFPflox/flox ESC lines before and after Cre mediated excision. Considerate that stable DNA methylation may remain upon Zfp961 absent, therefore ERVKs could still be repressed, we then treated Zfp961-GFPflox/flox cells with 5aza, which a inhibitor of DNA methylation, 24h before Zfp961 deletion with 4-OHT addition. After 4-OHT treatment，we performed RNAseq again, and this time we observed a ETnERV2-int, with belongs to ERVK elements, was upregulated after Zfp961 deletion.

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ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 repression capacity to transcription of ERVKs

Project description:ChIP-seq on Zfp961 GFP flox/flox mESCs to verify Zfp961 repression capacity to transcription of ERVKs

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ChIP-seq on Znf417 and Znf587 overexpression 293T to verify Znf417 and Znf587 binding capacity at PBS-Lys elements.

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