Smith B J, Yaffe M P
University of California, San Diego, Department of Biology, La Jolla 92093.
Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11091-4. doi: 10.1073/pnas.88.24.11091.
Exposure of cells to elevated temperatures causes a rapid increase in the synthesis of heat shock proteins (hsps) and induces thermotolerance, the increased ability of cells to survive exposure to lethal temperatures; however, the connection between hsp induction and the acquisition of thermotolerance is unclear. hsp induction in the yeast Saccharomyces cerevisiae is mediated by the activation of heat-shock transcription factor, and recently we have described a mutation, hsf1-m3, in heat-shock transcription factor that prevents the factor's activation. We now demonstrate that this mutation results in a general block in heat-shock induction but does not affect the acquisition of thermotolerance. Our results indicate that high-level induction of the major hsps is not required for cells to acquire thermotolerance.
将细胞暴露于高温下会导致热休克蛋白（hsps）的合成迅速增加，并诱导耐热性，即细胞在暴露于致死温度下存活能力的增强；然而，hsp诱导与耐热性获得之间的联系尚不清楚。酿酒酵母中的hsp诱导是由热休克转录因子的激活介导的，最近我们描述了热休克转录因子中的一种突变，即hsf1-m3，它可阻止该因子的激活。我们现在证明，这种突变会导致热休克诱导的普遍阻滞，但不影响耐热性的获得。我们的结果表明，细胞获得耐热性并不需要主要hsps的高水平诱导。
