A putative protein kinase overcomes pheromone-induced arrest of cell cycling in S. cerevisiae

Cell. 1989 Sep 22;58(6):1107-19. doi: 10.1016/0092-8674(89)90509-6.

Abstract

MATa cells carrying an sst2 mutation are unable to recover from the G1-specific cell cycle arrest induced by the mating pheromone alpha factor. The KSS1 gene, when overexpressed, suppresses this adaptation defect. KSS1 overexpression also suppresses the recovery defect manifested by cells expressing an alpha factor receptor lacking its 136 amino acid cytoplasmic tail. Because SST2 product and the receptor tail contribute independently to events that allow recovery from pheromone-induced growth arrest, KSS1 function defines a third independent process that promotes desensitization. The KSS1 gene encodes an apparent protein kinase homologous to the CDC28 (S. cerevisiae) and cdc2+ (S. pombe) gene products. The recovery-promoting activity of the KSS1 gene requires a functional WHI1 gene, which encodes a yeast homolog to animal cyclins, suggesting that the KSS1 and WHI1 proteins act in the same growth control pathway.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Base Sequence
  • Cell Cycle*
  • Chromosome Mapping
  • Genes*
  • Genes, Fungal*
  • Genotype
  • Mating Factor
  • Molecular Sequence Data
  • Mutation*
  • Peptides / genetics*
  • Pheromones / genetics*
  • Plasmids
  • Protein Kinases / metabolism*
  • Restriction Mapping
  • Saccharomyces cerevisiae / cytology
  • Saccharomyces cerevisiae / enzymology
  • Saccharomyces cerevisiae / genetics*
  • Sequence Homology, Nucleic Acid
  • Suppression, Genetic*

Substances

  • Peptides
  • Pheromones
  • Mating Factor
  • Protein Kinases

Associated data

  • GENBANK/M26398