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Vol. 12, No. 18, pp. 2943-2955, September 15, 1998
Botanisches Institut der Universität,
CH-4056 Basel, Switzerland
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.
[Key Words: Rim15p; protein kinase A; yeast; Ras; cAMP; nutrient signaling]
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