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Chromatin accessibility changes caused by expression of histone 3.3(K9M) in A375 cells

ABSTRACT: Chromatin accessibility changes caused by expression of histone 3.3(K9M) in A375 cells

PROVIDER: PRJNA800464 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17747993_1.fastq.gz	Fastqsanger.gz
	SRR17747993_2.fastq.gz	Fastqsanger.gz
	SRR17747994_1.fastq.gz	Fastqsanger.gz
	SRR17747994_2.fastq.gz	Fastqsanger.gz
	SRR17747995_1.fastq.gz	Fastqsanger.gz

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Gene expression changes caused by expression of histone 3.3(K9M) in A375 cells

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Chromatin accessibility changes caused by expression of histone 3.3(K9M) in A375 cells

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Piwi modulates chromatin accessibility by regulating multiple factors including histone H1 to repress transposons

Project description:PIWI-interacting RNAs (piRNAs) mediate transposable element (TE) silencing at the transcriptional or post-transcriptional level in animal gonads. In the Drosophila ovary, Piwiâ??piRNA complexes (Piwiâ??piRISCs) repress TE transcription by modifying the chromatin state, such as H3K9me3 marks. Here, we demonstrate that Piwi physically interacts with linker histone H1. Depletion of Piwi decreases H1 density on target loci, leading to TE derepression. Loss of H1 results in gain of chromatin accessibility at target loci without affecting H3K9me3 and heterochromatin protein 1a (HP1a) density at the same loci. Piwi-mediated TE silencing also requires HP1a by regulating chromatin accessibility through its association with target loci. Thus, Piwiâ??piRISCs require both H1 and HP1a to repress TEs, and the silencing is correlated with the state of chromatin formation rather than H3K9me3 marks. These findings suggest that Piwiâ??piRISCs regulate the interaction of chromatin components with target loci to maintain silencing of the TE state through the modulation of chromatin accessibility. RNA levels, H1 and H3K9me3 occupancy, chromatin accessibility, and Piwi-associated small RNA levels in ovarian somatic cells (OSC) depleted of piRNA pathway components and H1.

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