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

Induction of STE2 expression using the GAL1 promoter both in a wild-type MAT.alpha. strain and in a MAT.alpha. ste3 strain caused transient cell-cycle arrest and changes in morphology (''shmoo''-like phenotype) in a manner similar to a cells responding to .alpha.-factor. In addition, STE2 expressed in a MAT.alpha. ste3 mutant allowed the cell to conjugate with a cells but at an efficiency lower than that of wild-type .alpha. cells. This result indicates that signal(s) generated by a-factor in .alpha. cells can be substituted by signal(s) generated by the interaction of .alpha.-factor with the expressed STE2 product. When STE2 or STE3 was expressed in a mat.alpha.1 strain (insensitive to both .alpha.- and a-factors), the cell became sensitive to .alpha.- or a-factor, respectively, and resulted in morphological changes. These results suggest that STE2 and STE3 are the sole determinants for .alpha.-factor and a-factor sensitivity, respectively, in this strain. On the other hand, expression of STE2 in an a/.alpha. diploid cell did not affect the .alpha.-factor insensitive phenotype. Haploid-specific components may be necessary to transduce the .alpha.-factor signal. These results are consistent with the idea that STE2 encodes an .alpha.-factor receptor and STE3 encodes an a-factor receptor, and suggest that both .alpha.- and a-factors may generate an exchangeable signal(s) within haploid cells.