H2A.Z is dispensable for both basal and activated transcription in post-mitotic mouse muscles.


Journal

Nucleic acids research
ISSN: 1362-4962
Titre abrégé: Nucleic Acids Res
Pays: England
ID NLM: 0411011

Informations de publication

Date de publication:
21 05 2020
Historique:
accepted: 29 02 2020
revised: 06 02 2020
received: 14 11 2019
pubmed: 9 4 2020
medline: 9 9 2020
entrez: 9 4 2020
Statut: ppublish

Résumé

While the histone variant H2A.Z is known to be required for mitosis, it is also enriched in nucleosomes surrounding the transcription start site of active promoters, implicating H2A.Z in transcription. However, evidence obtained so far mainly rely on correlational data generated in actively dividing cells. We have exploited a paradigm in which transcription is uncoupled from the cell cycle by developing an in vivo system to inactivate H2A.Z in terminally differentiated post-mitotic muscle cells. ChIP-seq, RNA-seq and ATAC-seq experiments performed on H2A.Z KO post-mitotic muscle cells show that this histone variant is neither required to maintain nor to activate transcription. Altogether, this study provides in vivo evidence that in the absence of mitosis H2A.Z is dispensable for transcription and that the enrichment of H2A.Z on active promoters is a marker but not an active driver of transcription.

Identifiants

pubmed: 32266374
pii: 5816854
doi: 10.1093/nar/gkaa157
pmc: PMC7229818
doi:

Substances chimiques

Chromatin 0
H2az1 protein, mouse 0
Histones 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4601-4613

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.

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Auteurs

Edwige Belotti (E)

Institut NeuroMyoGène, Université Claude Bernard Lyon 1, Université de Lyon, INSERM U1217, CNRS UMR5310, 8 avenue Rockefeller, 69008 Lyon, France.

Nicolas Lacoste (N)

Institut NeuroMyoGène, Université Claude Bernard Lyon 1, Université de Lyon, INSERM U1217, CNRS UMR5310, 8 avenue Rockefeller, 69008 Lyon, France.

Thomas Simonet (T)

Institut NeuroMyoGène, Université Claude Bernard Lyon 1, Université de Lyon, INSERM U1217, CNRS UMR5310, 8 avenue Rockefeller, 69008 Lyon, France.

Christophe Papin (C)

Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, Parc d'innovation, 1 rue Laurent Fries, 67404 Ilkirch Cedex, France.

Kiran Padmanabhan (K)

Institut de Génomique Fonctionnelle de Lyon, CNRS UMR 5242, École Normale Supérieure de Lyon, Université Claude Bernard Lyon 1, 32-34 Avenue Tony Garnier, 69007 Lyon, France.

Isabella Scionti (I)

Institut NeuroMyoGène, Université Claude Bernard Lyon 1, Université de Lyon, INSERM U1217, CNRS UMR5310, 8 avenue Rockefeller, 69008 Lyon, France.

Yann-Gaël Gangloff (YG)

Institut NeuroMyoGène, Université Claude Bernard Lyon 1, Université de Lyon, INSERM U1217, CNRS UMR5310, 8 avenue Rockefeller, 69008 Lyon, France.

Lorrie Ramos (L)

Institute for Advanced Biosciences (IAB), Université Grenoble Alpes, CNRS UMR 5309, INSERM U1209, Site Santé - Allée des Alpes, 38700 La Tronche, France.

Defne Dalkara (D)

Institute for Advanced Biosciences (IAB), Université Grenoble Alpes, CNRS UMR 5309, INSERM U1209, Site Santé - Allée des Alpes, 38700 La Tronche, France.

Ali Hamiche (A)

Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, Parc d'innovation, 1 rue Laurent Fries, 67404 Ilkirch Cedex, France.

Stefan Dimitrov (S)

Institute for Advanced Biosciences (IAB), Université Grenoble Alpes, CNRS UMR 5309, INSERM U1209, Site Santé - Allée des Alpes, 38700 La Tronche, France.
Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Balcova, Izmir 35330, Turkey.

Laurent Schaeffer (L)

Institut NeuroMyoGène, Université Claude Bernard Lyon 1, Université de Lyon, INSERM U1217, CNRS UMR5310, 8 avenue Rockefeller, 69008 Lyon, France.
Centre de Biotechnologie Cellulaire, Hospices Civils de Lyon, Lyon, France.

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Classifications MeSH