Genetics, Vol. 157, 39-51, January 2001, Copyright © 2001

Genetic Evidence for a Morphogenetic Function of the Saccharomyces cerevisiae Pho85 Cyclin-Dependent Kinase

Marc E. Lenburga and Erin K. O'Sheaa
a Department of Biochemistry and Biophysics, University of California, San Francisco, California 94143-0448

Corresponding author: Erin K. O'Shea, Department of Biochemistry and Biophysics, University of California, 513 Parnassus Ave., Rm. S-960, San Francisco, CA 94143-0448., oshea{at}biochem.ucsf.edu (E-mail)

Communicating editor: M. JOHNSTON

The Saccharomyces cerevisiae PHO85 gene encodes a nonessential cyclin-dependent kinase that associates with 10 cyclin subunits. To survey the functions provided by Pho85, we identified mutants that require PHO85 for viability. We identified mutations that define seven Pho Eighty-Five Requiring or Efr loci, six of which are previously identified genes—BEM2 (YER155C), SPT7 (YBR081C), GCR1 (YPL075W), SRB5 (YGR104C), HFI1 (YPL254W), and BCK1 (YJL095W)—with one novel gene (YMR212C). We found that mutations in the EFR genes involved in morphogenesis are specifically inviable when the Pho85-associated G1 cyclins encoded by PCL1 and PCL2 are absent. pcl1{Delta} bem2, pcl1{Delta} pcl2{Delta} cla4{Delta}, and pcl1{Delta} pcl2{Delta} cdc42-1 strains are inviable. pcl1{Delta} pcl2{Delta} mpk1{Delta}, pcl1{Delta} pcl2{Delta} bck1, and pcl1{Delta} pcl2{Delta} cln1{Delta} cln2{Delta} strains are also inviable, but are rescued by osmotic stabilization with 1 M sorbitol. We propose that the G1 cyclins encoded by PCL1 and PCL2 positively regulate CDC42 or another morphogenesis promoting function.





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