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Distinct Contribution of DNA Methylation and Histone Acetylation to the Genomic Occupancy of Transcription Factors

ABSTRACT: Distinct Contribution of DNA Methylation and Histone Acetylation to the Genomic Occupancy of Transcription Factors

PROVIDER: PRJNA543349 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9074530_1.fastq.gz	Fastqsanger.gz
	SRR9074530_2.fastq.gz	Fastqsanger.gz
	SRR9074540_1.fastq.gz	Fastqsanger.gz
	SRR9074540_2.fastq.gz	Fastqsanger.gz
	SRR9074550_1.fastq.gz	Fastqsanger.gz

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Distinct Contribution of DNA Methylation and Histone Acetylation to the Genomic Occupancy of Transcription Factors

Project description:DNA methylation has been shown to act by directly modulating transcription factor affinity to DNA binding sites and by recruiting methyl-CpG binding proteins, which form complexes with histone deacetylases (HDACs). Both mechanisms can affect gene regulation, but the extent to which HDACs contribute to the function of DNA methylation and transcription factor occupancy is not clear. To address this question we measured gene expression alterations, chromatin accessibility and transcription factor occupancy in wild type or DNA methylation-deficient mouse embryonic stem cells following HDAC inhibition. We observe widespread elevated chromatin accessibility at repeat elements following histone hyper-acetylation, which was magnified by the absence of DNA methylation. Subsets of repeat elements displayed enriched binding by distinct transcription factors and elevated expression. The pronounced additive effect of HDAC inhibition in DNA methylation deficient cells demonstrate that DNA methylation and histone deacetylation act largely independently to supress transcription factor binding and gene expression.

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Distinct contributions of DNA methylation and histone acetylation to the genomic occupancy of transcription factors.

Project description:Epigenetic modifications on chromatin play important roles in regulating gene expression. Although chromatin states are often governed by multilayered structure, how individual pathways contribute to gene expression remains poorly understood. For example, DNA methylation is known to regulate transcription factor binding but also to recruit methyl-CpG binding proteins that affect chromatin structure through the activity of histone deacetylase complexes (HDACs). Both of these mechanisms can potentially affect gene expression, but the importance of each, and whether these activities are integrated to achieve appropriate gene regulation, remains largely unknown. To address this important question, we measured gene expression, chromatin accessibility, and transcription factor occupancy in wild-type or DNA methylation-deficient mouse embryonic stem cells following HDAC inhibition. We observe widespread increases in chromatin accessibility at retrotransposons when HDACs are inhibited, and this is magnified when cells also lack DNA methylation. A subset of these elements has elevated binding of the YY1 and GABPA transcription factors and increased expression. The pronounced additive effect of HDAC inhibition in DNA methylation-deficient cells demonstrates that DNA methylation and histone deacetylation act largely independently to suppress transcription factor binding and gene expression.

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Tuning Transcription Factor Availability through Acetylation-Mediated Genomic Redistribution

Project description:It is widely assumed that decreasing transcription factor DNA-binding affinity reduces transcription initiation by diminishing occupancy of sequence-specific regulatory elements. However in vivo transcription factors find their binding sites while confronted with a large excess of low affinity degenerate motifs. Here we show, using the melanoma lineage survival oncogene MITF as a model, that low affinity binding sites act as a competitive reservoir in vivo from which TFs are released by MAPK-stimulated acetylation to promote increased occupancy of their regulatory elements. Consequently a low DNA-binding affinity acetylation-mimetic MITF mutation supports melanocyte development and drives tumorigenesis, whereas a high affinity, non-acetylatable mutant does neither. The results reveal a paradoxical acetylation-mediated molecular clutch that tunes transcription factor availability via genome-wide titration and couples BRAF to tumorigenesis. Our results further suggest that genomic titration regulated by p300/CBP-mediated acetylation will represent a common mechanism to control TF availability.

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