Saltsman K A, Prentice H L, Kingston R E
Department of Molecular Biology, Massachusetts General Hospital, Boston 02114, USA.
Mol Gen Genet. 1999 Feb;261(1):161-9. doi: 10.1007/s004380050953.
Heat shock factor (hsf) is the transcriptional activator that governs the transcriptional response of eukaryotic cells to stressful conditions. The structure and regulation of hsf is highly conserved. We describe deletion mutations in hsf+ that alter the ability of Schizosaccharomyces pombe to respond to different stressful conditions. One mutation causes increased sensitivity to cadmium while maintaining near normal sensitivity to heat stress, while another mutation confers increased sensitivity to heat stress but retains normal sensitivity to cadmium. Despite the differential sensitivity of these two strains to cadmium and heat stress, the mutant hsf proteins in each strain were activated by both cadmium and heat. However, we found that these mutations differentially affected the ability of hsf to activate different promoters: one mutated hsf activated the ssp1+ gene better than the wis2+ gene following either stress, while the other mutated hsf activated wis2+ better than ssp1+. We propose that the differential ability of strains that contain these mutant hsfs to survive cadmium and heat stress is not caused by differences in activation of hsf, but is caused instead by differential abilities of the mutant hsfs to activate the appropriate sets of genes needed for survival.
热休克因子(hsf)是一种转录激活因子,它调控真核细胞对应激条件的转录反应。hsf的结构和调控高度保守。我们描述了hsf⁺中的缺失突变,这些突变改变了粟酒裂殖酵母对不同应激条件的反应能力。一种突变导致对镉的敏感性增加,而对热应激保持接近正常的敏感性,而另一种突变赋予对热应激的敏感性增加,但对镉保持正常敏感性。尽管这两种菌株对镉和热应激的敏感性不同,但每种菌株中的突变hsf蛋白都被镉和热激活。然而,我们发现这些突变对hsf激活不同启动子的能力有不同影响:一种突变的hsf在任何一种应激后激活ssp1⁺基因的能力都比wis2⁺基因强,而另一种突变的hsf激活wis2⁺基因的能力比ssp1⁺基因强。我们提出,含有这些突变hsf的菌株在镉和热应激下存活能力的差异不是由hsf激活的差异引起的,而是由突变hsf激活生存所需的适当基因集的能力差异引起的。