Oehlen L J, Cross F R
Rockefeller University, New York, New York 10021, USA.
J Biol Chem. 1998 Apr 10;273(15):8556-9. doi: 10.1074/jbc.273.15.8556.
The small G-protein Cdc42 functions in many eukaryotic signal transduction pathways. In the budding yeast Saccharomyces cerevisiae, cells with defective Cdc42 fail to induce mating-specific genes in response to mating factor and to adopt the proper morphology for conjugation. Here we show that the failure of mating factor-induced transcription is largely the indirect result of arrest at a specific cell cycle position and/or the accumulation of high levels of the Cln1/2-Cdc28 kinase, a known repressor of mating factor signal transduction. Cdc42-defective cells with restored transcriptional induction have a partially restored mating ability but are still defective in the morphological response to mating factor. These results show that Cdc42 is not required for transduction of the mating factor signal per se but that it is essential for proper mating factor-induced morphogenesis.
小G蛋白Cdc42在许多真核生物信号转导途径中发挥作用。在芽殖酵母酿酒酵母中，Cdc42有缺陷的细胞无法响应交配因子诱导交配特异性基因，也无法采用适当的形态进行接合。我们在此表明，交配因子诱导的转录失败很大程度上是细胞停滞在特定细胞周期位置和/或高水平Cln1/2-Cdc28激酶积累的间接结果，Cln1/2-Cdc28激酶是已知的交配因子信号转导抑制剂。转录诱导恢复的Cdc42缺陷细胞具有部分恢复的交配能力，但在对交配因子的形态反应中仍然存在缺陷。这些结果表明，Cdc42本身并非交配因子信号转导所必需，但对于交配因子诱导的正常形态发生至关重要。
