Role of SSD1 in Phenotypic Variation of Saccharomyces cerevisiae Strains Lacking DEG1-Dependent Pseudouridylation

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dc.date.accessioned2021-11-19T10:58:59Z
dc.date.available2021-11-19T10:58:59Z
dc.date.issued2021-08-15
dc.description.sponsorshipGefördert durch den Publikationsfonds der Universität Kassel
dc.identifierdoi:10.17170/kobra-202111195108
dc.identifier.urihttp://hdl.handle.net/123456789/13400
dc.language.isoeng
dc.relation.doidoi:10.3390/ijms22168753
dc.rightsNamensnennung 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectyeasteng
dc.subjectSSD1eng
dc.subjectpseudouridineeng
dc.subjecttRNA modificationeng
dc.subject.ddc630
dc.subject.swdTransfer-RNSger
dc.subject.swdModifizierungger
dc.subject.swdPseudouridinger
dc.titleRole of SSD1 in Phenotypic Variation of Saccharomyces cerevisiae Strains Lacking DEG1-Dependent Pseudouridylationeng
dc.typeAufsatz
dc.type.versionpublishedVersion
dcterms.abstractYeast phenotypes associated with the lack of wobble uridine (U34) modifications in tRNA were shown to be modulated by an allelic variation of SSD1, a gene encoding an mRNA-binding protein. We demonstrate that phenotypes caused by the loss of Deg1-dependent tRNA pseudouridylation are similarly affected by SSD1 allelic status. Temperature sensitivity and protein aggregation are elevated in deg1 mutants and further increased in the presence of the ssd1-d allele, which encodes a truncated form of Ssd1. In addition, chronological lifespan is reduced in a deg1 ssd1-d mutant, and the negative genetic interactions of the U34 modifier genes ELP3 and URM1 with DEG1 are aggravated by ssd1-d. A loss of function mutation in SSD1, ELP3, and DEG1 induces pleiotropic and overlapping phenotypes, including sensitivity against target of rapamycin (TOR) inhibitor drug and cell wall stress by calcofluor white. Additivity in ssd1 deg1 double mutant phenotypes suggests independent roles of Ssd1 and tRNA modifications in TOR signaling and cell wall integrity. However, other tRNA modification defects cause growth and drug sensitivity phenotypes, which are not further intensified in tandem with ssd1-d. Thus, we observed a modification-specific rather than general effect of SSD1 status on phenotypic variation in tRNA modification mutants. Our results highlight how the cellular consequences of tRNA modification loss can be influenced by protein targeting specific mRNAs.eng
dcterms.accessRightsopen access
dcterms.creatorKhonsari, Bahar
dcterms.creatorKlassen, Roland
dcterms.creatorSchaffrath, Raffael
dcterms.source.articlenumber8753
dcterms.source.identifiereissn:1422-0067
dcterms.source.issueIssue 16
dcterms.source.journalInternational journal of molecular scienceseng
dcterms.source.volumeVolume 22
kup.iskupfalse

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