Regulation of cytokinesis in the milk yeast Kluyveromyces lactis

DC FieldValueLanguage
dc.contributor.authorRippert, Dorthe
dc.contributor.authorHeppeler, Nele
dc.contributor.authorAlbermann, Sabine
dc.contributor.authorSchmitz, Hans-Peter
dc.contributor.authorHeinisch, Juergen J.
dc.date.accessioned2021-12-23T15:59:13Z-
dc.date.available2021-12-23T15:59:13Z-
dc.date.issued2014
dc.identifier.issn01674889
dc.identifier.urihttps://osnascholar.ub.uni-osnabrueck.de/handle/unios/3797-
dc.description.abstractCytokinesis in yeast and mammalian cells is a highly coordinated process mediated by the constriction of an actomyosin ring. In yeasts, it is accompanied by the formation of a chitinous primary septum. Although much is known about the regulation of cytokinesis in budding yeast, overlapping functions of redundant genes complicates genetic analyses. Here, we investigated the effects of various deletion mutants on cytokinesis in the milk yeast Kluyveromyces lactis. To determine the spatiotemporal parameters of cytokinesis components, live-cell imaging of fluorophor-tagged KlMyo1 and a new Lifeact probe for KlAct1 was employed. In contrast to Saccharomyces cerevisiae, where deletion of ScMYO1 is lethal, Klmyo1 deletion was temperature-sensitive. Transmission and scanning electron microscopy demonstrated that the Klmyo1 deletion cells had a defect in the formation of the primary septum and in cell separation; this result was confirmed by FACS analyses. Deletion of KlCYK3 was lethal, whereas in S. cerevisiae a cyk3 deletion is synthetically lethal with hof1 deletion. Growth of Klhof1 mutants was osmoremedial at 25 degrees C, as it is in S. cerevisiae. CYK3 and HOF1 genes cross-complemented in both species, suggesting that they are functional homologs. Inn1, a common interactor for these two regulators, was essential in both yeasts and the encoding genes did not cross-complement. The C2 domain of the Inn1 homologs conferred species specificity. Thus, our work establishes K. lactis as a model yeast to study cytokinesis with less genetic redundancy than S. cerevisiae. The viability of Klmyo1 deletions provides an advantage over budding yeast to study actomyosin-independent cytokinesis. Moreover, the lethality of Klcyk3 null mutants suggests that there are fewer functional redundancies with KlHof1 in K. lactis. (C) 2014 Elsevier B.V. All rights reserved.
dc.description.sponsorshipDeutsche ForschungsgemeinschaftGerman Research Foundation (DFG) [SFB 944]; We are grateful to Arne Jendretzki for providing a number of plasmids and strains related to cytokinesis regulators from S. cerevisiae. We also thank Bernadette Sander-Turgut and Andrea Murra for excellent technical support. This work was funded by a grant from the Deutsche Forschungsgemeinschaft (SFB 944).
dc.language.isoen
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofBIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
dc.subjectActin cytoskeleton
dc.subjectACTOMYOSIN RING
dc.subjectBAR PROTEIN HOF1
dc.subjectBiochemistry & Molecular Biology
dc.subjectBUDDING YEAST
dc.subjectCell Biology
dc.subjectCHITIN SYNTHASE
dc.subjectCLEAVAGE FURROW
dc.subjectCOLI SHUTTLE VECTORS
dc.subjectCYK3
dc.subjectDUAL FUNCTION
dc.subjectKINASE DBF2
dc.subjectSEPTUM FORMATION
dc.subjectYeast cytokinesis
dc.titleRegulation of cytokinesis in the milk yeast Kluyveromyces lactis
dc.typejournal article
dc.identifier.doi10.1016/j.bbamcr.2014.07.020
dc.identifier.isiISI:000342527800030
dc.description.volume1843
dc.description.issue11
dc.description.startpage2685
dc.description.endpage2697
dc.contributor.orcid0000-0001-5449-4593
dc.contributor.researcheridG-3801-2017
dc.identifier.eissn18792596
dc.publisher.placePO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
dcterms.isPartOf.abbreviationBiochim. Biophys. Acta-Mol. Cell Res.
dcterms.oaStatusBronze
crisitem.author.deptFB 05 - Biologie/Chemie-
crisitem.author.deptFB 05 - Biologie/Chemie-
crisitem.author.deptidfb05-
crisitem.author.deptidfb05-
crisitem.author.orcid0000-0001-5449-4593-
crisitem.author.parentorgUniversität Osnabrück-
crisitem.author.parentorgUniversität Osnabrück-
crisitem.author.netidRiDo775-
crisitem.author.netidScHa130-
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