How the Fus3 MAP kinase ensures signaling specificity during mating and filamentous growth in S. cerevisiae.
Marie Bao, Monica Schwartz, Hiten Madhani
Biochemistry and Biophysics, UCSF, 600 16th St. N374, San Francisco, CA, 94143, USA
The mating pathway-specific MAPK Fus3 prevents cross-talk between mating and filamentation pathways (Cell 91(5):673). In its absence, pheromone signaling erroneously activates haploid invasive growth and reporter genes driven by the filamentation response element (FRE), the target of the filamentation-specific heteromeric transcription factor Tec1-Ste12 (Science 275(5304):1314). The molecular mechanisms by which Fus3 prevents cross-talk has remained mysterious. We have now determined that one mechanism by which Fus3 prevents cross-talk is by promoting the rapid degradation of filamentation transcription factor Tec1. The inactivation of Tec1 is absolutely dependent on Fus3 since in fus3delete cells, Tec1 is stabilized in the absence of pheromone, and its levels remain unchanged upon pheromone stimulation. Mutation of a consensus MAP kinase phosphorylation site in Tec1 abolishes its degradation in response to pheromone signaling and also causes pheromone pathway-dependent activation of a FRE-lacZ reporter gene. Thus, Fus3- and pheromone-dependent regulation of Tec1 is necessary for signaling specificity. These results explain how specificity is maintained even though transcriptional activation of mating and filamentation specific genes both require the transcription factor subunit Ste12. In addition, they explain how specificity can be maintained despite some leaky phosphorylation of the filamentation MAP kinase Kss1 in response to mating pheromone (Mol Cell 8(3):683).
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