Rowley A, Johnston G C, Butler B, Werner-Washburne M, Singer R A
Department of Microbiology and Immunology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
Mol Cell Biol. 1993 Feb;13(2):1034-41. doi: 10.1128/mcb.13.2.1034-1041.1993.
For cells of the yeast Saccharomyces cerevisiae, heat shock causes a transient inhibition of the cell cycle-regulatory step START. We have determined that this heat-induced START inhibition is accompanied by decreased CLN1 and CLN2 transcript abundance and by possible posttranscriptional changes to CLN3 (WHI1/DAF1) cyclin activity. Persistent CLN2 expression from a heterologous promoter or the CLN2-1 or CLN3-1 alleles that are thought to encode cyclin proteins with increased stability eliminated heat-induced START inhibition but did not affect other aspects of the heat shock response. Heat-induced START inhibition was shown to be independent of functions that regulate cyclin activity under other conditions and of transcriptional regulation of SWI4, an activator of cyclin transcription. Cells lacking Bcy1 function and thus without cyclic AMP control of A kinase activity were inhibited for START by heat shock as long as A kinase activity was attenuated by mutation. We suggest that heat shock mediates START blockage through effects on the G1 cyclins.
对于酿酒酵母细胞而言,热激会导致细胞周期调控步骤START的短暂抑制。我们已经确定,这种热诱导的START抑制伴随着CLN1和CLN2转录本丰度的降低以及CLN3(WHI1/DAF1)细胞周期蛋白活性可能的转录后变化。来自异源启动子的持续CLN2表达或被认为编码稳定性增加的细胞周期蛋白的CLN2-1或CLN3-1等位基因消除了热诱导的START抑制,但不影响热激反应的其他方面。热诱导的START抑制被证明独立于在其他条件下调节细胞周期蛋白活性的功能以及细胞周期蛋白转录激活因子SWI4的转录调控。缺乏Bcy1功能因而没有A激酶活性的环磷酸腺苷控制的细胞,只要A激酶活性因突变而减弱,热激就会抑制START。我们认为热激通过对G1期细胞周期蛋白的作用介导START阻滞。