Chang E C, Kosman D J, Willsky G R
Department of Biochemistry, State University of New York, Buffalo 14214.
J Bacteriol. 1989 Nov;171(11):6349-52. doi: 10.1128/jb.171.11.6349-6352.1989.
The growth response of Saccharomyces cerevisiae to arsenite and arsenate and the relationship between the enhancement of heat shock protein (hsp) synthesis caused by these arsenic oxides and thermotolerance are reported. Arsenite and arsenate transiently inhibited cell growth and overall protein synthesis; arsenate enhanced the synthesis of the 42-, 74-, 84-, and 100-kilodalton hsps, whereas arsenite enhanced synthesis of only the 74-kilodalton hsp. The induction of these hsps reached a maximum 45 min following metal oxide treatment and then declined. A delayed thermotolerance peaked 4 h after metal oxide addition, at which time cell growth and protein synthesis were recovering. These data show that the arsenate- and arsenite-induced thermotolerance in S. cerevisiae cells does not appear to be causally related to either hsp synthesis or cell cycle arrest.
报道了酿酒酵母对亚砷酸盐和砷酸盐的生长反应，以及这些氧化砷引起的热休克蛋白（hsp）合成增强与耐热性之间的关系。亚砷酸盐和砷酸盐短暂抑制细胞生长和总体蛋白质合成；砷酸盐增强了42、74、84和100千道尔顿hsp的合成，而亚砷酸盐仅增强了74千道尔顿hsp的合成。这些hsp的诱导在金属氧化物处理后45分钟达到最大值，然后下降。延迟的耐热性在添加金属氧化物后4小时达到峰值，此时细胞生长和蛋白质合成正在恢复。这些数据表明，酿酒酵母细胞中砷酸盐和亚砷酸盐诱导的耐热性似乎与hsp合成或细胞周期停滞没有因果关系。
