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Mol Cell. 2016 Aug 4;63(3):408-19. doi: 10.1016/j.molcel.2016.06.008. Epub 2016 Jul 14.

Piwi Modulates Chromatin Accessibility by Regulating Multiple Factors Including Histone H1 to Repress Transposons.

Author information

1
Department of Molecular Biology, Keio University School of Medicine, Tokyo 160-8582, Japan.
2
Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo 113-0032, Japan.
3
Department of Molecular Biology, Keio University School of Medicine, Tokyo 160-8582, Japan. Electronic address: awa403@keio.jp.
4
Department of Molecular Biology, Keio University School of Medicine, Tokyo 160-8582, Japan. Electronic address: saito@z6.keio.jp.

Abstract

PIWI-interacting RNAs (piRNAs) mediate transcriptional and post-transcriptional silencing of transposable element (TE) in animal gonads. In Drosophila ovaries, Piwi-piRNA complexes (Piwi-piRISCs) repress TE transcription by modifying the chromatin state, such as by H3K9 trimethylation. Here, we demonstrate that Piwi physically interacts with linker histone H1. Depletion of Piwi decreases H1 density at a subset of TEs, leading to their derepression. Silencing at these loci separately requires H1 and H3K9me3 and heterochromatin protein 1a (HP1a). Loss of H1 increases target loci chromatin accessibility without affecting H3K9me3 density at these loci, while loss of HP1a does not impact H1 density. Thus, Piwi-piRISCs require both H1 and HP1a to repress TEs, and the silencing is correlated with the chromatin state rather than H3K9me3 marks. These findings suggest that Piwi-piRISCs regulate the interaction of chromatin components with target loci to maintain silencing of TEs through the modulation of chromatin accessibility.

PMID:
27425411
DOI:
10.1016/j.molcel.2016.06.008
[Indexed for MEDLINE]
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