The Mi-2 nucleosome remodeler and the Rpd3 histone deacetylase are involved in piRNA-guided heterochromatin formation.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
04 06 2020
Historique:
received: 07 11 2018
accepted: 11 05 2020
entrez: 6 6 2020
pubmed: 6 6 2020
medline: 19 8 2020
Statut: epublish

Résumé

In eukaryotes, trimethylation of lysine 9 on histone H3 (H3K9) is associated with transcriptional silencing of transposable elements (TEs). In drosophila ovaries, this heterochromatic repressive mark is thought to be deposited by SetDB1 on TE genomic loci after the initial recognition of nascent transcripts by PIWI-interacting RNAs (piRNAs) loaded on the Piwi protein. Here, we show that the nucleosome remodeler Mi-2, in complex with its partner MEP-1, forms a subunit that is transiently associated, in a MEP-1 C-terminus-dependent manner, with known Piwi interactors, including a recently reported SUMO ligase, Su(var)2-10. Together with the histone deacetylase Rpd3, this module is involved in the piRNA-dependent TE silencing, correlated with H3K9 deacetylation and trimethylation. Therefore, drosophila piRNA-mediated transcriptional silencing involves three epigenetic effectors, a remodeler, Mi-2, an eraser, Rpd3 and a writer, SetDB1, in addition to the Su(var)2-10 SUMO ligase.

Identifiants

pubmed: 32499524
doi: 10.1038/s41467-020-16635-5
pii: 10.1038/s41467-020-16635-5
pmc: PMC7272611
doi:

Substances chimiques

Argonaute Proteins 0
Autoantigens 0
Drosophila Proteins 0
Heterochromatin 0
Histones 0
Mi-2 protein, Drosophila 0
Nucleosomes 0
Protein Inhibitors of Activated STAT 0
RNA, Small Interfering 0
Su(var)2-10 protein, Drosophila 0
HDAC1 protein, Drosophila EC 3.5.1.98
Histone Deacetylase 1 EC 3.5.1.98
Adenosine Triphosphatases EC 3.6.1.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2818

Subventions

Organisme : NIH HHS
ID : P40 OD010949
Pays : United States

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Auteurs

Bruno Mugat (B)

Institute of Human Genetics, UMR9002, CNRS and Univ. Montpellier, Montpellier, France.

Simon Nicot (S)

Institute of Human Genetics, UMR9002, CNRS and Univ. Montpellier, Montpellier, France.

Carolina Varela-Chavez (C)

Institute of Human Genetics, UMR9002, CNRS and Univ. Montpellier, Montpellier, France.

Christophe Jourdan (C)

Institute of Human Genetics, UMR9002, CNRS and Univ. Montpellier, Montpellier, France.

Kaoru Sato (K)

Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.

Eugenia Basyuk (E)

Institute of Human Genetics, UMR9002, CNRS and Univ. Montpellier, Montpellier, France.

François Juge (F)

Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France.

Mikiko C Siomi (MC)

Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.

Alain Pélisson (A)

Institute of Human Genetics, UMR9002, CNRS and Univ. Montpellier, Montpellier, France.

Séverine Chambeyron (S)

Institute of Human Genetics, UMR9002, CNRS and Univ. Montpellier, Montpellier, France. severine.chambeyron@igh.cnrs.fr.

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