Common signal transduction system shared by STE2 and STE3 in haploid cells of Saccharomyces cerevisiae: autocrine cell-cycle arrest results from forced expression of STE2

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Induction of STE2 expression using the GAL1 promoter both in a wild-type MATα strain and in a MATα ste3 strain caused transient cell-cycle arrest and changes in morphology (`shmoo'-like phenotype) in a manner similar to a cells responding to α-factor. In addition, STE2 expressed in a MATα ste3 mutant allowed the cell to conjugate with a cells but at an efficiency lower than that of wild-type α cells. This result indicates that signal(s) generated by a-factor in α cells can be substituted by signal(s) generated by the interaction of α-factor with the expressed STE2 product. When STE2 or STE3 was expressed in a matα1 strain (insensitive to both α- and a-factors), the cell became sensitive to α- or a-factor, respectively, and resulted in morphological changes. These results suggest that STE2 and STE3 are the sole determinants for α-factor and a-factor sensitivity, respectively, in this strain. On the other hand, expression of STE2 in an a/α diploid cell did not affect the α-factor insensitive phenotype. Haploid-specific components may be necessary to transduce the α-factor signal. These results are consistent with the idea that STE2 encodes an α-factor receptor and STE3 encodes an a-factor receptor, and suggest that both α- and a-factors may generate an exchangeable signal(s) within haploid cells.

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