The small G-protein Cdc42 functions in many eukaryotic signal transduction pathways. In the budding yeast Saccharomyces cerevisiae, cells with defective Cdc42 fail to induce mating-specific genes in response to mating factor and to adopt the proper morphology for conjugation. Here we show that the failure of mating factor-induced transcription is largely the indirect result of arrest at a specific cell cycle position and/or the accumulation of high levels of the Cln1/2-Cdc28 kinase, a known repressor of mating factor signal transduction. Cdc42 defective cells with restored transcriptional induction have a partially restored mating ability but are still defective in the morphological response to mating factor. These results show that Cdc42 is not required for transduction of the mating factor signal per se but that it is essential for proper mating factor-induced morphogenesis.
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Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA
Kyushu Univ, Grad Sch Med Sci, Fukuoka, JapanUniv Penn, Perelman Sch Med, Philadelphia, PA 19104 USA
Okada, Satoshi
Lee, Mid Eum
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Ohio State Univ, Columbus, OH 43210 USA
Geisel Sch Med Dartmouth, Dept Biochem & Cell Biol, Hanover, NH 03755 USAUniv Penn, Perelman Sch Med, Philadelphia, PA 19104 USA
Lee, Mid Eum
Bi, Erfei
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Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USAUniv Penn, Perelman Sch Med, Philadelphia, PA 19104 USA
Bi, Erfei
Park, Hay-Oak
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Ohio State Univ, Columbus, OH 43210 USAUniv Penn, Perelman Sch Med, Philadelphia, PA 19104 USA