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The SAS-Chromatin Remodeling Complex Mediates Inflorecence-Specific Chromatin Accessibility for Transcription Factor Binding

ABSTRACT: The SAS-Chromatin Remodeling Complex Mediates Inflorecence-Specific Chromatin Accessibility for Transcription Factor Binding

PROVIDER: PRJNA1071262 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27792872.fastq.gz	Fastqsanger.gz
	SRR27792873.fastq.gz	Fastqsanger.gz
	SRR27792874.fastq.gz	Fastqsanger.gz
	SRR27792875.fastq.gz	Fastqsanger.gz
	SRR27792876.fastq.gz	Fastqsanger.gz

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The SAS-Chromatin Remodeling Complex Mediates Inflorecence-Specific Chromatin Accessibility for Transcription Factor Binding [ChIP-Seq]

Project description:The SAS-Chromatin Remodeling Complex Mediates Inflorecence-Specific Chromatin Accessibility for Transcription Factor Binding [ChIP-Seq]

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The SAS-Chromatin Remodeling Complex Mediates Inflorecence-Specific Chromatin Accessibility for Transcription Factor Binding [ChIP-Seq]

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Acute BAF perturbation causes immediate changes in chromatin accessibility

Project description:Loss-of-function mutations in genes coding for subunits of the large, multifarious BRG1/BRM associated factor (BAF) chromatin remodeling complexes are frequently causative for cancer or developmental diseases1-5. Cells lacking the most frequently mutated subunits like the ATPase SMARCA4 typically exhibit drastic chromatin accessibility changes, especially of important regulatory regions6-12. However, so far it remains unknown how these changes are established over time, and whether they are causative for intra-complex synthetic lethalities abrogating the formation (SMARCC1-SMARCC2)8,13,14 or activity (SMARCA4-SMARCA2)15-17 of BAF complexes. Here, we utilize the dTAG system18 to induce acute degradation of BAF subunits in wild-type and BAF mutant backgrounds and analyze the resulting chromatin accessibility changes with high kinetic resolution. We observe that chromatin alterations are established faster than the duration of one cell cycle and that maintaining genome accessibility requires constant ATP-dependent remodeling. Completely abolishing BAF complex function by acute degradation of a synthetic lethal subunit in a paralog-deficient background results in a near-complete loss of chromatin accessibility at BAF-controlled sites, especially at super-enhancers, providing a mechanism for intra-complex synthetic lethalities.

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Project description:The tissue-specific packaging of the genome into the nucleus through chromatin is fundamentally involved in gene regulation, and aberrant modifications to chromatin are a hallmark of many diseases. We show here that a high fat (HF) diet leads to substantial chromatin remodeling in the livers of C57BL/6J mice, as compared to mice fed a control diet. Regions of the genome that display the greatest variation in chromatin accessibility between HF and control regions are targeted by transcription factors with known roles in the liver including HNF4α, CEBP/α, and FOXA1. Whereas livers of DBA/2J mice fed a HF or control diet also demonstrate diet-induced chromatin remodeling, the regions displaying the greatest variation are largely distinct from those observed in B6 livers, indicating a crosstalk between genetic and epigenetic components in determining how diet-induced chromatin remodeling is associated with metabolic disease progression. Examination of chromatin remodeling with FAIRE-seq in livers of mice (C57BL/6J and DBA/2J) fed a high fat or control diet. Complemented with gene expression and H3K4me1 analyses

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