Hog1 activation delays mitotic exit via phosphorylation of Net1

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• dc.contributor.author Tognetti, Silvia
• dc.contributor.author Jiménez, Javier
• dc.contributor.author Viganò, Matteo
• dc.contributor.author Duch, Alba
• dc.contributor.author Queralt Badia, Ethel
• dc.contributor.author Nadal Clanchet, Eulàlia de
• dc.contributor.author Posas Garriga, Francesc
• dc.date.accessioned 2020-05-06T07:10:51Z
• dc.date.available 2020-05-06T07:10:51Z
• dc.date.issued 2020
• dc.description.abstract Adaptation to environmental changes is crucial for cell fitness. In Saccharomyces cerevisiae, variations in external osmolarity trigger the activation of the stress-activated protein kinase Hog1 (high-osmolarity glycerol 1), which regulates gene expression, metabolism, and cell-cycle progression. The activation of this kinase leads to the regulation of G1, S, and G2 phases of the cell cycle to prevent genome instability and promote cell survival. Here we show that Hog1 delays mitotic exit when cells are stressed during metaphase. Hog1 phosphorylates the nucleolar protein Net1, altering its affinity for the phosphatase Cdc14, whose activity is essential for mitotic exit and completion of the cell cycle. The untimely release of Cdc14 from the nucleolus upon activation of Hog1 is linked to a defect in ribosomal DNA (rDNA) and telomere segregation, and it ultimately delays cell division. A mutant of Net1 that cannot be phosphorylated by Hog1 displays reduced viability upon osmostress. Thus, Hog1 contributes to maximizing cell survival upon stress by regulating mitotic exit.
• dc.description.sponsorship The study was supported by grants from the Spanish Ministry of Economy and Competitiveness (PGC2018-094136-B-I00 to F.P.; BFU2017-85152-P and FEDER to E.d.N.; BFU2016-77975-R and FEDER to E.Q.), the Catalan Government (2017 SGR 799), and Fundación Botín, by Banco Santander through its Santander Universities Global Division (to F.P.). We gratefully acknowledge institutional funding from the Spanish Ministry of Economy, Industry and Competitiveness (MINECO) through the Centres of Excellence Severo Ochoa Award, and from the CERCA Programme of the Catalan Government and the Unidad de Excelencia María de Maeztu, funded by the AEI (CEX2018-000792-M). F.P. is the recipient of an ICREA Acadèmia Award (Generalitat de Catalunya).
• dc.format.mimetype application/pdf
• dc.identifier.citation Tognetti S, Jiménez J, Viganò M, Duch A, Queralt E, de Nadal E, Posas F. Hog1 activation delays mitotic exit via phosphorylation of Net1. Proc Natl Acad Sci U S A. 2020; 117(16):8924-33. DOI: 10.1073/pnas.1918308117
• dc.identifier.doi http://dx.doi.org/10.1073/pnas.1918308117
• dc.identifier.issn 0027-8424
• dc.identifier.uri http://hdl.handle.net/10230/44425
• dc.language.iso eng
• dc.publisher National Academy of Sciences
• dc.relation.ispartof Proc Natl Acad Sci U S A. 2020; 117(16):8924-33
• dc.relation.projectID info:eu-repo/grantAgreement/ES/2PE/PGC2018-094136-B-I00
• dc.relation.projectID info:eu-repo/grantAgreement/ES/2PE/BFU2017-85152-P
• dc.relation.projectID info:eu-repo/grantAgreement/ES/1PE/BFU2016-77975-R
• dc.rights © 2020 the Author(s). Published by PNAS. This open access article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/
• dc.subject.keyword MAPK
• dc.subject.keyword Net1
• dc.subject.keyword Cell cycle
• dc.subject.keyword Mitosis
• dc.subject.keyword Osmostress
• dc.title Hog1 activation delays mitotic exit via phosphorylation of Net1
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion