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H4K16ac activates retrotransposons and contributes to their cis regulatory function [ATAC-seq]

ABSTRACT: H4K16ac activates retrotransposons and contributes to their cis regulatory function [ATAC-seq]

PROVIDER: PRJNA826523 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18746449_1.fastq.gz	Fastqsanger.gz
	SRR18746449_2.fastq.gz	Fastqsanger.gz
	SRR18746450_1.fastq.gz	Fastqsanger.gz
	SRR18746450_2.fastq.gz	Fastqsanger.gz
	SRR18746451_1.fastq.gz	Fastqsanger.gz

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H4K16ac activates retrotransposons and contributes to their cis regulatory function

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H4K16ac activates retrotransposons and contributes to their cis regulatory function [CUT&TAG]

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H4K16ac activates retrotransposons and contributes to their cis regulatory function [RNA-seq]

Project description:Mammalian genomes harbour a large number of transposable elements (TEs) and their remnants. Most TEs are incapable of retrotransposition, however, they have evolved as cis-regulatory elements (CREs), enabling them to recruit host-encoded factors. Understanding the contribution of TEs in the regulation of the mammalian genome is an active area of research. Here we show that the male-specific lethal (MSL) complex-mediated acetylation of histone H4 lysine 16 (H4K16ac) regulates the transcription of TEs. Furthermore, H4K16ac marked TEs function as a rich source of cis regulatory elements in the human genome, wherein H4K16ac acts by maintaining the permissive chromatin structure and promoting the transcription of these TEs.

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H4K16ac activates retrotransposons and contributes to their cis regulatory function [CUT&TAG]

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H4K16ac activates retrotransposons and contributes to their cis regulatory function [ATAC-seq]

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H4K16ac activates retrotransposons and contributes to their cis regulatory function

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H4K16ac activates the transcription of transposable elements and contributes to their cis-regulatory function.

Project description:Mammalian genomes harbor abundant transposable elements (TEs) and their remnants, with numerous epigenetic repression mechanisms enacted to silence TE transcription. However, TEs are upregulated during early development, neuronal lineage, and cancers, although the epigenetic factors contributing to the transcription of TEs have yet to be fully elucidated. Here, we demonstrate that the male-specific lethal (MSL)-complex-mediated histone H4 acetylation at lysine 16 (H4K16ac) is enriched at TEs in human embryonic stem cells (hESCs) and cancer cells. This in turn activates transcription of subsets of full-length long interspersed nuclear elements (LINE1s, L1s) and endogenous retrovirus (ERV) long terminal repeats (LTRs). Furthermore, we show that the H4K16ac-marked L1 and LTR subfamilies display enhancer-like functions and are enriched in genomic locations with chromatin features associated with active enhancers. Importantly, such regions often reside at boundaries of topologically associated domains and loop with genes. CRISPR-based epigenetic perturbation and genetic deletion of L1s reveal that H4K16ac-marked L1s and LTRs regulate the expression of genes in cis. Overall, TEs enriched with H4K16ac contribute to the cis-regulatory landscape at specific genomic locations by maintaining an active chromatin landscape at TEs.

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