DNA methylation and histone H1 jointly repress transposable elements and aberrant intragenic transcripts
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA504886 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10100200.fastq.gz | Fastqsanger.gz | |||
| SRR10100201.fastq.gz | Fastqsanger.gz | |||
| SRR10100202.fastq.gz | Fastqsanger.gz | |||
| SRR10100203.fastq.gz | Fastqsanger.gz | |||
| SRR10100204.fastq.gz | Fastqsanger.gz |
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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, Piwi–piRNA complexes (Piwi–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, Piwi–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 Piwi–piRISCs regulate the interaction of chromatin components with target loci to maintain silencing of the TE state through the modulation of chromatin accessibility.
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