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Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers

ABSTRACT: Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers

PROVIDER: PRJNA246702 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1283440_1.fastq.gz	Fastqsanger.gz
	SRR1283440_2.fastq.gz	Fastqsanger.gz
	SRR1283450_1.fastq.gz	Fastqsanger.gz
	SRR1283450_2.fastq.gz	Fastqsanger.gz
	SRR1283351.fastq.gz	Fastqsanger.gz

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Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [MNase-Seq]

Project description:In higher eukaryotes, enhancers and promoters share many properties, including binding of transcription factors, existing in open chromatin, and bidirectional transcription. Yet the structural features that distinguish enhancers and promoters are unclear. Genome-wide micrococcal nuclease (MNase) studies previously interpreted MNase hypersensitivity to indicate that active enhancers and promoters are nucleosome-free, yet other studies found histone variants and post-translational modifications at active enhancers. We find that prior MNase genomic studies have an overdigestion bias and that low-level MNase digestion, coupled with mapping core histones, reveals two classes of MNase-hypersensitive sites: at active promoters, which are nucleosome depleted, and at tissue-specific enhancers, which retain core histones and co-bound transcription factors substantially more than promoters. Hypersensitivity of active enhancer nucleosomes may reflect their preferential exposure in chromatin and can be maintained by pioneer transcription factors such as FoxA. These findings unveil fundamental differences in the chromatin structure of active enhancers and promoters.

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Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [ChIP-Seq]

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Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [ChIP-exo]

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Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers

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

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Histone octamer structure is altered early in ISW2 ATP-dependent remodeling of nucleosomes

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Project description:Enhancers act to regulate cell type specific gene expression by facilitating the transcription of target genes. In mammalian cells active or primed enhancers are commonly marked by monomethylation of Histone H3 at lysine 4 (H3K4me1) in a cell-type specific manner. Whether and how this histone modification regulates enhancer-dependent transcription programs in mammals has been unclear. In the present study, we conducted SILAC Mass-spec experiments with mono-nucleosomes and identified multiple H3K4me1 associated proteins, including proteins involved in chromatin remodeling. We demonstrate that H3K4me1 augments the association of the chromatin remodeling complex BAF to enhancers in vivo. Furthermore we show that in vitro, H3K4me1 nucleosomes are more efficiently remodeled by the BAF complex. Crystal structures of a BAF component BAF45c further reveal that monomethylation, but not trimethylation, is accommodated in this protein’s H3K4 binding site. Our results suggest that H3K4me1 plays an active role at enhancers by facilitating the binding of the BAF complex and possibly other chromatin regulators.

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Project description:Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [ChIP-Seq]

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Project description:Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [ChIP-exo]

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Mus musculus

Project description:Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [MNase-Seq]

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