title: A role for the Swe1 checkpoint kinase during filamentous growth of Saccharomyces cerevisiae.
abstract: In this study we show that inactivation of Hsl1 or Hsl7, negative regulators of the Swe1 kinase, enhances the invasive behavior of haploid and diploid cells. The enhancement of filamentous growth caused by inactivation of both genes is mediated via the Swe1 protein kinase. Whereas Swe1 contributes noticeably to the effectiveness of haploid invasive growth under all conditions tested, its contribution to pseudohyphal growth is limited to the morphological response under standard assay conditions. However, Swe1 is essential for pseudohyphal differentiation under a number of nonstandard assay conditions including altered temperature and increased nitrogen. Swe1 is also required for pseudohyphal growth in the absence of Tec1 and for the induction of filamentation by butanol, a related phenomenon. Although inactivation of Hsl1 is sufficient to suppress the defect in filamentous growth caused by inactivation of Tec1 or Flo8, it is insufficient to promote filamentous growth in the absence of both factors. Moreover, inactivation of Hsl1 will not bypass the requirement for nitrogen starvation or growth on solid medium for pseudohyphal differentiation. We conclude that the Swe1 kinase modulates filamentous development under a broad spectrum of conditions and that its role is partially redundant with the Tec1 and Flo8 transcription factors.
authors.affiliation: Departments of Molecular Biology and Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Rd., La Jolla, CA 92037, USA.
authors.forename: R
authors.initials: R
authors.lastname: La Valle
authors.forename: C
authors.initials: C
authors.lastname: Wittenberg
mesh_terms: D018797:Cell Cycle Proteins; D002455:Cell Division; D000242:Cyclic AMP / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D004171:Diploidy; D004789:Enzyme Activation; D005656:Fungal Proteins / Q000378:metabolism; D005838:Genotype; D006238:Haploidy; D009154:Mutation; D009584:Nitrogen / Q000378:metabolism; D009687:Nuclear Proteins; D010641:Phenotype; D010957:Plasmids; D011494:Protein Kinases / Q000235:genetics; D017346:Protein Serine-Threonine Kinases; D011484:Protein-Arginine N-Methyltransferases; D011505:Protein-Tyrosine Kinases / Q000235:genetics* / Q000502:physiology*; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins; D013696:Temperature; D013997:Time Factors; D015534:Trans-Activators / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; C100940:FLO8 protein, S cerevisaie; D005656:Fungal Proteins; D009687:Nuclear Proteins; D029701:Saccharomyces cerevisiae Proteins; C069926:TEC1 protein, S cerevisiae; D015534:Trans-Activators; D014157:Transcription Factors; D000242:Cyclic AMP; D011484:Protein-Arginine N-Methyltransferases; C120666:HSL7 protein, S cerevisiae; D011494:Protein Kinases; C099685:SWE1 protein, S cerevisiae; D011505:Protein-Tyrosine Kinases; C106494:HSL1 protein, S cerevisiae; D017346:Protein Serine-Threonine Kinases; D009584:Nitrogen