Dolan J W
Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29425, USA.
Curr Genet. 1996 Dec;30(6):469-75. doi: 10.1007/s002940050158.
Saccharomyces cerevisiae responds to pheromones by arresting cell-cycle progression at the G1/S boundary. This arrest has been shown to require the activation by phosphorylation of Far1, a cyclin-dependent kinase inhibitor. Arrest resembling pheromone-induced arrest can be triggered by high levels of Ste12, the pheromone-responsive transcriptional activator. In the present study, cell-cycle arrest induced by high levels of Ste12 is characterized. This arrest occurs predominately at the G1/S boundary and is independent of Far1 and upstream components of the pheromone response pathway. Since Ste12 is a transcriptional activator, it is proposed that cell-cycle arrest in response to high levels of Ste12 is due to transcription of a Ste12-dependent arrest factor regulated primarily, but not necessarily exclusively, at the level of transcription. The data presented here suggest that a novel component has a role in arrest in response to pheromone.
酿酒酵母通过在G1/S边界阻滞细胞周期进程来响应信息素。这种阻滞已被证明需要细胞周期蛋白依赖性激酶抑制剂Far1通过磷酸化激活。高水平的信息素应答转录激活因子Ste12可引发类似于信息素诱导的阻滞。在本研究中,对高水平Ste12诱导的细胞周期阻滞进行了表征。这种阻滞主要发生在G1/S边界,且独立于Far1和信息素应答途径的上游成分。由于Ste12是一种转录激活因子,因此有人提出,对高水平Ste12的细胞周期阻滞是由于一种主要但不一定完全在转录水平调控的Ste12依赖性阻滞因子的转录。此处呈现的数据表明,一种新成分在对信息素的阻滞中起作用。