Unger M W, Hartwell L H
Proc Natl Acad Sci U S A. 1976 May;73(5):1664-8. doi: 10.1073/pnas.73.5.1664.
We suggest that two events are necessary for an asynchronous population of cells to undergo arrest in the GI phase of the cell cycle upon nutrient starvation. First, passage through GI must be prevented by a deficiency of some metabolic intermediate. Since this intermediate may act indirectly to arrest division, we designate it the "signal". We have found three conditions under which Saccharomyces cerevisiae cells arrest division in GI: sulfate starvation of a prototroph, methionine starvation of an auxotroph, or a shift of a conditional methionyl-tRNA synthetase mutant [L-methionine: tRNA Met ligase (AMP-forming), EC 6.1.1.10] to a restrictive condition. We interpret these results to indicate that the signal for sulfate starvation in S. cerevisiae is generated near the end of the sulfate assimilation pathway (at or beyond the formation of mehtionyl-tRNA). As a unifying hypothesis, we propose that the signal for all nutrients is generated at the level of protein biosynthesis.
我们认为,对于一群异步细胞在营养饥饿时在细胞周期的G1期发生停滞,有两个事件是必要的。首先,某些代谢中间产物的缺乏必须阻止细胞通过G1期。由于这种中间产物可能间接作用以阻止分裂,我们将其称为“信号”。我们发现了三种酿酒酵母细胞在G1期停止分裂的情况:原养型细胞的硫酸盐饥饿、营养缺陷型细胞的甲硫氨酸饥饿,或条件性甲硫氨酰 - tRNA合成酶突变体[L - 甲硫氨酸:tRNA Met连接酶(形成AMP),EC 6.1.1.10]转变到限制条件。我们对这些结果的解释是,酿酒酵母中硫酸盐饥饿的信号是在硫酸盐同化途径接近末端(在甲硫氨酰 - tRNA形成时或之后)产生的。作为一个统一的假设,我们提出所有营养物质的信号都是在蛋白质生物合成水平产生的。