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Pkc1 acts through Zds1 and Gic1 to suppress growth and cell polarity defects of a yeast eIF5A mutant

dc.contributor.authorZanelli, Cleslei Fernando [UNESP]
dc.contributor.authorValentini, Sandro Roberto [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:24:40Z
dc.date.available2014-05-20T13:24:40Z
dc.date.issued2005-12-01
dc.description.abstracteIF5A is a highly conserved putative eukaryotic translation initiation factor that has been implicated in translation initiation, nucleocytoplasmic transport, mRNA decay, and cell proliferation, but with no precise function assigned so far. We have previously shown that high-copy PKCI suppresses the phenotype of tif51A-1, a temperature-sensitive mutant of eIF5A in S. cerevisiae. Here, in an attempt to further understand how Pkc1 functionally interacts with eIF-5A, it was determined that PKCI suppression of tif51A-1 is independent of the cell integrity MAP kinase cascade. Furthermore, two new suppressor genes, ZDS1 and GIC1, were identified. We demonstrated that ZDS1 and ZDS2 are necessary for PKC1, but not for GIC1 suppression. Moreover, high-copy GIC1 also suppresses the growth defect of a PKCI mutant (stt1), suggesting the existence of a Pkc1-Zds1-Gic1 pathway. Consistent with the function of Gic1 in actin organization, the tif51A-1 strain shows an actin polarity defect that is partially recovered by overexpression of Pkc1 and Zds1 as well as Gic1. Additionally, PCL1 and BNI1, important regulators of yeast cell polarity, also suppress tif51A-1 temperature sensitiviiy Taken together, these data strongly Support the correlated involvement of Pkc1 and eIF5A in establishing actin polarity, which is essential for bud formation and G1/S transition in S. cerevisiae.en
dc.description.affiliationSão Paulo State Univ, Sch Pharmaceut Sci, Dept Biol Sci, UNESP, BR-14801902 Araraquara, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Sch Pharmaceut Sci, Dept Biol Sci, UNESP, BR-14801902 Araraquara, SP, Brazil
dc.format.extent1571-1581
dc.identifierhttp://dx.doi.org/10.1534/genetics.105.048082
dc.identifier.citationGenetics. Bethesda: Genetics Soc Am, v. 171, n. 4, p. 1571-1581, 2005.
dc.identifier.doi10.1534/genetics.105.048082
dc.identifier.issn0016-6731
dc.identifier.lattes5333250355049814
dc.identifier.lattes1525665408900195
dc.identifier.orcid0000-0001-7831-1149
dc.identifier.urihttp://hdl.handle.net/11449/7734
dc.identifier.wosWOS:000234407100013
dc.language.isoeng
dc.publisherGenetics Soc Am
dc.relation.ispartofGenetics
dc.relation.ispartofjcr4.075
dc.relation.ispartofsjr3,484
dc.rights.accessRightsAcesso restritopt
dc.sourceWeb of Science
dc.titlePkc1 acts through Zds1 and Gic1 to suppress growth and cell polarity defects of a yeast eIF5A mutanten
dc.typeArtigopt
dcterms.licensehttp://www.genetics.org/site/misc/ifora.xhtml#POLICY%20ON%20PRE-PRINT%20DEPOSITS
dcterms.rightsHolderGenetics Soc Am
dspace.entity.typePublication
relation.isDepartmentOfPublication5004bcab-94af-4939-b980-091ae9d0a19e
relation.isDepartmentOfPublication.latestForDiscovery5004bcab-94af-4939-b980-091ae9d0a19e
relation.isOrgUnitOfPublication95697b0b-8977-4af6-88d5-c29c80b5ee92
relation.isOrgUnitOfPublication.latestForDiscovery95697b0b-8977-4af6-88d5-c29c80b5ee92
unesp.author.lattes5333250355049814
unesp.author.lattes1525665408900195[1]
unesp.author.orcid0000-0001-7831-1149[1]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Ciências Farmacêuticas, Araraquarapt
unesp.departmentCiências Biológicas - FCFpt

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