Konopka J B
Department of Microbiology, State University of New York at Stony Brook 11794-5222.
Mol Cell Biol. 1993 Nov;13(11):6876-88. doi: 10.1128/mcb.13.11.6876-6888.1993.
Mating pheromone receptors activate a G-protein signaling pathway that induces changes in transcription, cell division, and morphogenesis needed for the conjunction of Saccharomyces cerevisiae. The C terminus of the alpha-factor pheromone receptor functions in two complex processes, adaptation and morphogenesis. Adaptation to alpha-factor may occur through receptor desensitization, and alpha-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 alpha-factor. Unexpectedly, cells lacking AFR1 showed a defect in alpha-factor-stimulated morphogenesis that was similar to the morphogenesis defect observed in cells producing C-terminally truncated alpha-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.
交配信息素受体激活一种G蛋白信号通路，该通路可诱导酿酒酵母接合所需的转录、细胞分裂和形态发生变化。α-因子信息素受体的C末端在两个复杂过程中发挥作用，即适应性和形态发生。对α-因子的适应可能通过受体脱敏发生，并且α-因子诱导的形态发生形成了交配细胞之间的接合桥。采用质粒过表达策略分离出一个新基因AFR1，它与受体C末端共同作用以促进适应性。AFR1的表达受到α-因子的高度诱导。出乎意料的是，缺乏AFR1的细胞在α-因子刺激的形态发生方面存在缺陷，这与在产生C末端截短的α-因子受体的细胞中观察到的形态发生缺陷相似。相反，AFR1的过表达导致形态发生的突起更长，这表明该基因可能直接刺激形态发生。这些结果表明AFR1编码一种受发育调控的功能，该功能在接合过程中协调受体信号传导的调节和形态发生的诱导。
