FB2026_02 , released June 18, 2026
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Citation
Iwasaki, Y.W., Murano, K., Ishizu, H., Shibuya, A., Iyoda, Y., Siomi, M.C., Siomi, H., Saito, K. (2016). Piwi Modulates Chromatin Accessibility by Regulating Multiple Factors Including Histone H1 to Repress Transposons.  Mol. Cell 63(3): 408--419.
FlyBase ID
FBrf0233069
Publication Type
Research paper
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.
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Obtained with permission from Cell Press.
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Mol. Cell
    Title
    Molecular Cell
    Publication Year
    1997-
    ISBN/ISSN
    1097-2765 1097-4164
    Data From Reference
    Genes (5)
    Physical Interactions (6)
    Cell Lines (1)
    Natural transposons (6)