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dc.contributor.authorColomina i Gabarrella, Neus
dc.contributor.authorFerrezuelo, Francisco
dc.contributor.authorVergés, Emili
dc.contributor.authorAldea, Martí
dc.contributor.authorGarí Marsol, Eloi
dc.date.accessioned2017-01-25T10:03:14Z
dc.date.issued2009
dc.identifier.issn1538-4101
dc.identifier.urihttp://hdl.handle.net/10459.1/59109
dc.description.abstractThe Whi3 protein is associated with the endoplasmic reticulum, interacts with Cdc28, the budding-yeast Cdk, binds the mRNA of cyclin CLN3 and prevents accumulation of the Cdc28-Cln3 in the nucleus until late G1. Besides its function as a cell size regulator, Whi3 is strictly required for filamentous growth. Here we show that emerging buds in Whi3-deficient cells are considerably rounder than in wild-type cells, indicating that Whi3 is required to maintain apical growth during S phase. This defect was not suppressed by deletion of CLB2, which is involved in switching from polar to isotropic bud growth, indicating that the observed phenotype is not the result of Whi3 acting solely as a negative regulator of cyclin Clb2. However, Cdc28 did not properly accumulate at the bud tip during S phase in whi3Δ cells, and their elongation defects were suppressed by CLN2 overexpression, suggesting a positive function for Whi3 in a Cdk-cyclin-dependent step required for apical growth. Additionally, the actin cytoskeleton was perturbed in Whi3- deficient cells, and WHI3 showed genetic interactions with actin patch components. Our results point to Whi3 as a key modulator of apical growth effectors to coordinate cell cycle events and morphogenesis. We propose that Whi3 is required for the apical localization of Cdc28-Cln1,2 complexes during bud growth and thereby, to promote the activation of Cdc42 and its effectors in the bud apex.ca_ES
dc.description.sponsorshipWe thank Sònia Rius and Isis Navarro for their technical assistance. We gratefully acknowledge Yoshimi Takai, Enrico Cabib, Erin O’Shea, Michael Hall, Vladimir Voynov, Gerald Fink, Humberto Torres, María Molina, Barbara Winsor, Carlos Vázquez de Aldana, Kelly Tedrick and Gary Eitzen for yeast strains and plasmids. We also thank Jordi Torres and Carme Gallego for critically reading the manuscript. Thanks also go to the members of CYC lab for helpful discussions. This work was funded by the Ministry of Science and Innovation of Spain (Consolider-Ingenio 2010), Fundació La Caixa, and the European Union (FEDER). N.C. and F.F. are researchers of the Ramon y Cajal program. E.V. received a fellowship from Generalitat de Catalunya.ca_ES
dc.language.isoengca_ES
dc.publisherLandes Bioscienceca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.4161/cc.8.12.8740ca_ES
dc.relation.ispartofCell Cycle, 2009, vol. 8, núm. 12, p. 1912-1920ca_ES
dc.rights(c) Landes Bioscience, 2009ca_ES
dc.subjectSaccharomyces cerevisiaeca_ES
dc.subjectWhi3ca_ES
dc.subjectApical growthca_ES
dc.subjectMorphogenesisca_ES
dc.subjectCdkca_ES
dc.subjectG1 cyclinca_ES
dc.titleWhi3 regulates morphogenesis in budding yeast by enhancing Cdk functions in apical growthca_ES
dc.typearticleca_ES
dc.identifier.idgrec013408
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.4161/cc.8.12.8740
dc.date.embargoEndDate2025-01-01


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