Ensa controls S-phase length by modulating Treslin levels

Sophie Charrasse, Aicha Gharbi-Ayachi, Andrew Burgess, Jorge Vera, Khaled Hached, Peggy Raynaud, Etienne Schwob, Thierry Lorca () and Anna Castro ()
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Sophie Charrasse: Université de Montpellier, Centre de Recherche de Biologie Cellulaire de Montpellier, Equipe Labellisée ‘Ligue Contre le Cancer’, CNRS UMR 5237
Aicha Gharbi-Ayachi: Université de Montpellier, Centre de Recherche de Biologie Cellulaire de Montpellier, Equipe Labellisée ‘Ligue Contre le Cancer’, CNRS UMR 5237
Andrew Burgess: Garvan Institute of Medical Research
Jorge Vera: Université de Montpellier, Centre de Recherche de Biologie Cellulaire de Montpellier, Equipe Labellisée ‘Ligue Contre le Cancer’, CNRS UMR 5237
Khaled Hached: Université de Montpellier, Centre de Recherche de Biologie Cellulaire de Montpellier, Equipe Labellisée ‘Ligue Contre le Cancer’, CNRS UMR 5237
Peggy Raynaud: Université de Montpellier, Centre de Recherche de Biologie Cellulaire de Montpellier, Equipe Labellisée ‘Ligue Contre le Cancer’, CNRS UMR 5237
Etienne Schwob: CNRS UMR 5535, University of Montpellier
Thierry Lorca: Université de Montpellier, Centre de Recherche de Biologie Cellulaire de Montpellier, Equipe Labellisée ‘Ligue Contre le Cancer’, CNRS UMR 5237
Anna Castro: Université de Montpellier, Centre de Recherche de Biologie Cellulaire de Montpellier, Equipe Labellisée ‘Ligue Contre le Cancer’, CNRS UMR 5237

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract The Greatwall/Ensa/PP2A-B55 pathway is essential for controlling mitotic substrate phosphorylation and mitotic entry. Here, we investigate the effect of the knockdown of the Gwl substrate, Ensa, in human cells. Unexpectedly, Ensa knockdown promotes a dramatic extension of S phase associated with a lowered density of replication forks. Notably, Ensa depletion results in a decrease of Treslin levels, a pivotal protein for the firing of replication origins. Accordingly, the extended S phase in Ensa-depleted cells is completely rescued by the overexpression of Treslin. Our data herein reveal a new mechanism by which normal cells regulate S-phase duration by controlling the ubiquitin-proteasome degradation of Treslin in a Gwl/Ensa-dependent pathway.

Date: 2017
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DOI: 10.1038/s41467-017-00339-4

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