AFR1 acts in conjunction with the α-factor receptor to promote morphogenesis and adaptation

Mating pheromone receptors activate a G-protein signaling pathway that induces changes in transcription, cell division, and morphogenesis needed for the conjugation of Saccharomyces cerevisiae. The C terminus of the α-factor pheromone receptor functions in two complex processes, adaptation and morphogenesis. Adaptation to α-factor may occur through receptor desensitization, and α-factor-induced morphogenesis forms the conjugation bridge between mating cells. A plasmid overexpression strategy was used to isolate a new gene, AFR1, which acts together with the receptor C terminus to promote adaptation. The expression of AFR1 was highly induced by α-factor. Unexpectedly, cells lacking AFR1 showed a defect in α -factor-stimulated morphogenesis that was similar to the morphogenesis defect observed in cells producing C-terminally truncated α-factor receptors. In contrast, AFR1 overexpression resulted in longer projections of morphogenesis, which suggests that this gene may directly stimulate morphogenesis. These results indicate that AFR1 encodes a developmentally regulated function that coordinates both the regulation of receptor signaling and the induction of morphogenesis during conjugation.