| Title: | 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 |
| Author(s): | Nakayama N; Miyajima A; Arai K; |
| Address: | "Department of Molecular Biology, DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304, USA" |
| DOI: | 10.1002/j.1460-2075.1987.tb04746.x |
| ISSN/ISBN: | 0261-4189 (Print) 1460-2075 (Electronic) 0261-4189 (Linking) |
| Abstract: | "Induction of STE2 expression using the GAL1 promoter both in a wild-type MATalpha strain and in a MATalpha ste3 strain caused transient cell-cycle arrest and changes in morphology ('shmoo'-like phenotype) in a manner similar to alpha cells responding to alpha-factor. In addition, STE2 expressed in a MATalp[ha ste3 mutant allowed the cell to conjugate with alpha cells but at an efficiency lower than that of wil-type alpha cells. This result indicates that signal(s) generated by alpha-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 matalpha1 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" |
| Keywords: | "Cell Cycle/*genetics Gene Expression Regulation, Fungal/genetics Haploidy Phenotype Plasmids/genetics Receptors, G-Protein-Coupled/*genetics Receptors, Mating Factor Receptors, Peptide/*genetics Receptors, Pheromone/*genetics Saccharomyces cerevisiae/*gen;" |
| Notes: | "MedlineNakayama, N Miyajima, A Arai, K eng Research Support, Non-U.S. Gov't England 1987/01/01 EMBO J. 1987 Jan; 6(1):249-54. doi: 10.1002/j.1460-2075.1987.tb04746.x" |
