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Hangover regulates gene expression by limiting NSL-mediated H4K16 acetylation

ABSTRACT: Hangover regulates gene expression by limiting NSL-mediated H4K16 acetylation

PROVIDER: PRJEB88170 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14825323.fastq.gz	Fastqsanger.gz
	ERR14825324.fastq.gz	Fastqsanger.gz
	ERR14825325.fastq.gz	Fastqsanger.gz
	ERR14825326.fastq.gz	Fastqsanger.gz
	ERR14825327.fastq.gz	Fastqsanger.gz

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Evolutionary conserved NSL complex/BRD4 axis controls transcription activation via histone acetylation

Project description:Cells rely on a diverse repertoire of genes for maintaining homeostasis, but the transcriptional networks underlying their expression remain poorly understood. The MOF acetyltransferase-containing Non-Specific Lethal (NSL) complex is a broad transcription regulator. It is essential in Drosophila and haploinsufficiency of the human KANSL1 subunit results in the Koolen-de Vries syndrome. Here, we perform a genome-wide RNAi screen and identify the BET protein BRD4 as evolutionary conserved co-factor of the NSL complex. Using Drosophila and mouse embryonic stem cells, we characterise a recruitment hierarchy, where NSL-deposited histone acetylation induces BRD4 recruitment for transcription of constitutively active genes. Transcriptome analyses in Koolen-de Vries patient-derived fibroblasts reveals perturbations with a cellular homeostasis signature that are evoked by the NSL complex/BRD4-axis. We propose that BRD4 represents a conserved bridge between the NSL complex and transcription activation and provide a new perspective in the understanding of their functions in healthy and diseased states.

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Evolutionary conserved NSL complex/BRD4 axis controls transcription activation via histone acetylation

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H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction (I) [ChIP-Seq]

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H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction (II) [ChIP-Seq]

Project description:We report that acetylation of H4K16 is a new marker of active enhancers and that some enhancers are marked by H3K4me1, MOF and H4K16ac but not by acetylated H3K27 or p300, suggesting that they are novel p300-independent regulatory elements. ChIP-seq for H4K16 acetylation in undifferentiated 46c(sox1-gfp) ES cells, and FACS sorted day 5 Neural Progenitor Cells (differentiated with NB27 and Neuro2 medium supplements) , along with MNase digested input for both samples

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Genome-wide enrichment of Gcn5 and H3K18/H4K16 acetylation under physiological change of stress adaptation and stress recovery

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