PHYSIOLOGICAL CHARACTERIZATION OF SACCHAROMYCES-CEREVISIAE MUTANTS SUPER-SENSITIVE TO G1 ARREST BY A-FACTOR AND ALPHA-FACTOR PHEROMONES
PHYSIOLOGICAL CHARACTERIZATION OF SACCHAROMYCES-CEREVISIAE MUTANTS SUPER-SENSITIVE TO G1 ARREST BY A-FACTOR AND ALPHA-FACTOR PHEROMONES
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DOI：
10.1128/mcb.2.1.21
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发表时间：
1982-01-01
影响因子：
5.3
通讯作者：
OTTE, CA
中科院分区：
文献类型：
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作者：
CHAN, RK;OTTE, CA
S.在sst 1或sst 2中携带突变的酿酒酵母MATa细胞对由α.因子信息素当sst 1突变体与正常SST+细胞混合时，整个群体一起从α恢复。因子阻滞，表明SST+细胞帮助sst 1突变体恢复。互补试验和连锁分析表明，sst 1和bar 1，一种消除MATa细胞作为α-葡聚糖扩散屏障的能力的突变，在相同的基因中有病变。sst 1突变体可能在从α的恢复方面存在缺陷。因为它们不能降解信息素。在混合实验中，SST+细胞的存在不会增强Sst 2突变体的恢复。当将正常MATa细胞或携带sst 1或sst 2缺陷的突变细胞暴露于α.因子作用1小时，然后洗去信息素，SST 2细胞随后在α.比SST+或sst 1细胞长得多的时间。显然，sst 2突变体中的缺陷是细胞固有的，并参与α-淀粉酶的机制。在信息素与细胞的初始相互作用之后的某个步骤中的因子作用。Sst 2突变的存在似乎会导致生长衰弱，因为单倍体Sst 2 -1菌株的重复连续传代培养导致了生长更快的回复突变体的积累，这些回复突变体具有信息素抗性并且是交配缺陷的（不育）。
S. cerevisiae MATa cells carrying mutations in either sst1 or sst2 are supersensitive to the G1 arrest induced by .alpha. factor pheromone. When sst1 mutants were mixed with normal SST+ cells, the entire population recovered together from .alpha. factor arrest, suggesting that SST+ cells helped sst1 mutants to recover. Complementation tests and linkage analysis showed that sst1 and bar1, a mutation which eliminates the ability of MATa cells to act as a barrier to the diffusion of .alpha. factor, were lesions in the same genes. sst1 mutants may be defective in recovery from .alpha. factor arrest because they are unable to degrade the pheromone. Recovery of sst2 mutants was not potentiated by the presence of SST+ cells in mixing experiments. When either normal MATa cells or mutant cells carrying defects in sst1 or sst2 were exposed to .alpha. factor for 1 h and then washed free of the pheromone, the sst2 cells subsequently remained arrested in the absence of .alpha. factor for a much longer time than SST+ or sst1 cells. Apparently, the defect in sst2 mutants is intrinsic to the cell and is involved in the mechanism of .alpha. factor action at some step after the initial interaction of the pheromone with the cell. The presence of an sst2 mutation appears to cause a growth debility, since repeated serial subculture of haploid sst2-1 strains led to the accumulation of faster-growing revertants that were pheromone resistant and were mating defective (sterile).