Coordination mechanisms of stress response with cell cycle regulation by the yeast Pho85 kinase

当酵母细胞遇到环境压力时，细胞周期的进展被推迟，为适应压力条件提供了时间。我们发现CLN2在碱性条件下表达下调，而Pho85-Pho80复合体需要在碱性条件下维持CLN2的表达。我们还发现，Pho4是适应碱性条件所必需的，可能是通过激活Ptk2。碱性胁迫信号通过Pho81CKI来抑制Pho85-Pho80的活性，从而导致转录因子Pho4、Rim101和Crz1的激活，当过量生产时，所有这些转录因子都会抑制CLN2的表达。WHI5抑制CLN2的表达，当过量生产Pho85-Pcl9抑制Whi5的活性时，在Pho85Pho4rim101crz1四重缺失突变体中CLN2的表达水平被刺激。Rpd3通过这些因素参与了对CLN2的抑制。

When yeast cells encounter environmental stress, progression through the cell cycle is delayed, providing time for adaptation to the stress conditions. We found that CLN2 was downregulated under alkaline conditions, and that the Pho85-Pho80 complex was required to sustain CLN2 expression under alkaline conditions. We also found that Pho4 is necessary for adaptation to alkaline conditions, possibly by activating Ptk2. The alkaline stress signal was transmitted through Pho81 CKI to repress the Pho85-Pho80 activity, which leads to activation of transcription factors Pho4, Rim101, and Crz1, all of which inhibited CLN2 expression when overproduced. Whi5 represses CLN2 expression, and CLN2 expression level in a pho85 pho4 rim101 crz1 quadruple deletion mutant was stimulated when the Whi5 activity was repressed by overproduction of Pho85-Pcl9. Rpd3 is involved in CLN2 repression by these factors.