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Vol. 12, No. 18, pp. 2874-2886, September 15, 1998
Department of Biochemistry and Biophysics, University of California,
San Francisco, San Francisco, California 94143-0448 USA
The MAPKKK Ste11p functions in three Saccharomyces
cerevisiae MAPK cascades [the high osmolarity glycerol (HOG),
pheromone response, and pseudohyphal/invasive growth
pathways], but its activation in response to high osmolarity
stimulates only the HOG pathway. To determine what restricts
cross-activation of MAPK cascades (cross talk), we have studied mutants
in which the pheromone response pathway is activated by high osmolarity
(1 M sorbitol). We found that mutations in the HOG1
gene, encoding the p38-type MAPK of the HOG pathway, and in the
PBS2 gene, encoding the activating kinase for Hog1p, allowed
osmolarity-induced activation of the pheromone response pathway. This
cross talk required the osmosensor Sho1p, as well as Ste20p, Ste50p,
the pheromone response MAPK cascade (Ste11p, Ste7p, and Fus3p or
Kss1p), and Ste12p but not Ste4p or the MAPK scaffold protein, Ste5p.
The cross talk in hog1 mutants induced multiple responses of
the pheromone response pathway: induction of a FUS1::lacZ
reporter, morphological changes, and mating in ste4 and
ste5 mutants. We suggest that Hog1p may prevent osmolarity-induced cross talk by inhibiting Sho1p, perhaps as part of a
feedback control on the HOG pathway. We have also shown that Ste20p and
Ste50p function in the Sho1p branch of the HOG pathway and that a
second osmosensor in addition to Sho1p may activate Ste11p. Finally, we
have found that pseudohyphal growth exhibited by wild-type
(HOG1) strains depends on SHO1, suggesting that Sho1p
may be a receptor that feeds into the pseudohyphal growth pathway.
[Key Words: Hog1; MAP kinase; yeast pheromone response; yeast high osmolarity response; HOG pathway; signal transduction]
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