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Genome-wide maps of H3K27ac and H2A.Zac in HeLa K cells after depletion of PWWP2A by siRNA-mediated knockdown.

ABSTRACT: Genome-wide maps of H3K27ac and H2A.Zac in HeLa K cells after depletion of PWWP2A by siRNA-mediated knockdown.

PROVIDER: PRJNA433201 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6677650.fastq.gz	Fastqsanger.gz
	SRR6677641.fastq.gz	Fastqsanger.gz
	SRR6677651.fastq.gz	Fastqsanger.gz
	SRR6677642.fastq.gz	Fastqsanger.gz
	SRR6677652.fastq.gz	Fastqsanger.gz

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Genome-wide maps of H3K27ac and H2A.Zac in HeLa K cells after depletion of PWWP2A by siRNA-mediated knockdown.

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Project description:Transcriptional regulation by chromatin is a highly dynamic process directed through the recruitment and coordinated action of epigenetic modifiers and readers of these modifications. Using an unbiased proteomic approach to find interactors of H3K36me3, a modification enriched on active chromatin, here we identify PWWP2A and HDAC2 among the top interactors. PWWP2A and its paralog PWWP2B form a stable complex with NuRD subunits MTA1/2/3:HDAC1/2:RBBP4/7, but not with MBD2/3, p66α/β, and CHD3/4. PWWP2A competes with MBD3 for binding to MTA1, thus defining a new variant NuRD complex that is mutually exclusive with the MBD2/3-containing NuRD. In mESCs, PWWP2A/B is most enriched at highly transcribed genes. Loss of PWWP2A/B leads to increases in histone acetylation predominantly at highly expressed genes, accompanied by decreases in Pol II elongation. Collectively, these findings suggest a role for PWWP2A/B in regulating transcription through the fine-tuning of histone acetylation dynamics at actively transcribed genes.

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