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NCoR/SMRT co-repressors cooperate with c-MYC to create an epigenetic barrier to somatic cell reprogramming

ABSTRACT: NCoR/SMRT co-repressors cooperate with c-MYC to create an epigenetic barrier to somatic cell reprogramming

PROVIDER: PRJNA289459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2096650.fastq.gz	Fastqsanger.gz
	SRR2096670.fastq.gz	Fastqsanger.gz
	SRR2096651.fastq.gz	Fastqsanger.gz
	SRR2096661.fastq.gz	Fastqsanger.gz
	SRR2096671.fastq.gz	Fastqsanger.gz

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NCoR/SMRT co-repressors cooperate with c-MYC to create an epigenetic barrier to somatic cell reprogramming [RNA-seq]

Project description:Changing the somatic cell transcriptome to a pluripotent state using exogenous reprogramming factors needs transcriptional co-regulators that help activate or suppress gene expression and rewrite the epigenome. Here, we show that reprogramming-specific engagement of the NCoR/SMRT co-repressor complex at key pluripotency loci creates an epigenetic block to reprogramming. HDAC3 executes the repressive function of NCoR/SMRT in reprogramming by inducing histone deacetylation at these loci. Recruitment of NCoR/SMRT-HDAC3 to pluripotency genes is facilitated by all 4 Yamanaka factors (OCT4, SOX2, KLF4 and c-MYC) but mostly by c-MYC. Class IIa HDACs further potentiate this recruitment by interacting with both the reprogramming factors and NCoR/SMRT. Consequently, depleting NCoR/SMRT-HDAC3 function enables high efficiency of reprogramming, while elevating NCoR/SMRT-HDAC3 recruitment at pluripotency loci by over-expressing constitutively active class IIa HDACs derails it. Our findings thus uncover an unexpected epigenetic mechanism involving c-MYC, whose manipulation greatly enhances reprogramming efficiency.

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NCoR/SMRT co-repressors cooperate with c-MYC to create an epigenetic barrier to somatic cell reprogramming [ChIP-Seq]

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Project description:We detected an interaction between checkpoint kinase Chk2 and some members of the NCOR/SMRT co-repressor complex. In order to study the role of gene repression in the checkpoint response to DNA damage, we performed RNA profiling in NCOR or SMRT knockdown cells after treztment with cisplatin. U2OS cells were transfected with siRNAs for NCOR or SMRT, grown for 2 days in complete medium, and then treated with 100 microM cisplatin (CDDP) for 6h. Biological duplicates were used for RNa profiling

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Project description:Using ChIP-seq, we reveal the SMRT and NCoR co-repressor cistromes, which each consist of over 30,000 half-shared binding sites. Moreover, we identify Bcl6-bound sub-cistromes for each co-repressor, which are strongly concentrated on NF-κB-driven inflammatory and tissue remodeling genes. These results reveal a critical role for Bcl6 and its corepressors SMRT and NCoR in the prevention of atherosclerosis and chronic inflammation. Identification of SMRT and NCoR binding sites in wild-type and Bcl6 knockout primary bone-marrow derived macrophages

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NCoR/SMRT co-repressors cooperate with c-MYC to create an epigenetic barrier to somatic cell reprogramming

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

2018-03-07 | GSE70740 | GEO