title: Saccharomyces cerevisiae cAMP-dependent protein kinase controls entry into stationary phase through the Rim15p protein kinase.
abstract: The Saccharomyces cerevisiae protein kinase Rim15p was identified previously as a stimulator of meiotic gene expression. Here, we show that loss of Rim15p causes an additional pleiotropic phenotype in cells grown to stationary phase on rich medium; this phenotype includes defects in trehalose and glycogen accumulation, in transcriptional derepression of HSP12, HSP26, and SSA3, in induction of thermotolerance and starvation resistance, and in proper G1 arrest. These phenotypes are commonly associated with hyperactivity of the Ras/cAMP pathway. Tests of epistasis suggest that Rim15p may act in this pathway downstream of the cAMP-dependent protein kinase (cAPK). Accordingly, deletion of RIM15 suppresses the growth defect of a temperature-sensitive adenylate-cyclase mutant and, most importantly, renders cells independent of cAPK activity. Conversely, overexpression of RIM15 suppresses phenotypes associated with a mutation in the regulatory subunit of cAPK, exacerbates the growth defect of strains compromised for cAPK activity, and partially induces a starvation response in logarithmically growing wild-type cells. Biochemical analyses reveal that cAPK-mediated in vitro phosphorylation of Rim15p strongly inhibits its kinase activity. Taken together, these results place Rim15p immediately downstream and under negative control of cAPK and define a positive regulatory role of Rim15p for entry into both meiosis and stationary phase.
authors.affiliation: Botanisches Institut der Universität, CH-4056 Basel, Switzerland.
authors.forename: A
authors.initials: A
authors.lastname: Reinders
authors.forename: N
authors.initials: N
authors.lastname: Bürckert
authors.forename: T
authors.initials: T
authors.lastname: Boller
authors.forename: A
authors.initials: A
authors.lastname: Wiemken
authors.forename: C
authors.initials: C
authors.lastname: De Virgilio
mesh_terms: D001483:Base Sequence; D003001:Cloning, Molecular; D017868:Cyclic AMP-Dependent Protein Kinases / Q000235:genetics / Q000502:physiology*; D017931:DNA Primers / Q000235:genetics; D016193:G1 Phase; D017353:Gene Deletion; D015870:Gene Expression; D005800:Genes, Fungal; D008540:Meiosis; D008954:Models, Biological; D009154:Mutation; D010641:Phenotype; D010766:Phosphorylation; D016133:Polymerase Chain Reaction; D011494:Protein Kinases / Q000502:physiology*; D012441:Saccharomyces cerevisiae / Q000166:cytology* / Q000201:enzymology* / Q000235:genetics; D015398:Signal Transduction
chemical_list: D017931:DNA Primers; D011494:Protein Kinases; D017868:Cyclic AMP-Dependent Protein Kinases