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Recruitment of HMGN By H3K27ac Modified Nucleosomes to Regulatory Sites Modulates Transcription Factor Binding to Chromatin

ABSTRACT: Recruitment of HMGN By H3K27ac Modified Nucleosomes to Regulatory Sites Modulates Transcription Factor Binding to Chromatin

PROVIDER: PRJNA658791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12502900_1.fastq.gz	Fastqsanger.gz
	SRR12502900_2.fastq.gz	Fastqsanger.gz
	SRR12502825.fastq.gz	Fastqsanger.gz
	SRR12502826.fastq.gz	Fastqsanger.gz
	SRR12502827.fastq.gz	Fastqsanger.gz

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Recruitment of HMGN By H3K27ac Modified Nucleosomes to Regulatory Sites Modulates Transcription Factor Binding to Chromatin

Project description:H3K27ac modified nucleosomes are a major epigenetic mark of active chromatin that can be used to identify cell type specific chromatin regulatory regions which serve as binding sites for transcription factors. Here we show that H3K27ac modified nucleosomes recruit the ubiquitous nucleosome binding proteins HMGN1 and HMGN2 to cell-type specific chromatin regulatory regions. We find that HMGNs bind directly to the acetylated nucleosome and that the H3K27ac residue and linker DNA are necessary and sufficient for the preferential binding of HMGNs to the modified nucleosomes. Loss of HMGNs increases the levels of H3K27me3 and the histone H1 occupancy at enhancers and promoters and alters the interaction of several transcription factors with chromatin. These experiments identify an additional mechanism whereby the H3K27ac epigenetic mark promotes chromatin decompaction and provide insights into the molecular mechanism whereby HMGN proteins, which bind to chromatin without DNA sequence specificity, modulate cell type specific gene expression.

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