Susek R E, Lindquist S
Department of Molecular Genetics and Cell Biology, Howard Hughes Medical Institute, University of Chicago, Illinois 60637.
Mol Cell Biol. 1990 Dec;10(12):6362-73. doi: 10.1128/mcb.10.12.6362-6373.1990.
hsp26, the small heat shock protein of Saccharomyces cerevisiae, accumulates in response to heat and other types of stress. It also accumulates during the normal course of development, as cells enter stationary phase growth or begin to sporulate (S. Kurtz, J. Rossi, L. Petko, and S. Lindquist, Science 231:1154-1157, 1986). Analysis of deletion and insertion mutations demonstrated that transcriptional control plays a critical role in regulating HSP26 expression. The HSP26 promoter was found to be complex and appears to contain repressing elements as well as activating elements. Several upstream deletion mutations resulted in strong constitutive expression of HSP26. Furthermore, upstream sequences from the HSP26 gene repressed the constitutive expression of a heterologous heat shock gene. We propose that basal repression and heat-induced depression of transcription play major roles in regulating the expression of HSP26. None of the recombinant constructs that we analyzed separated cis-regulatory sequences responsible for heat shock regulation from those responsible for developmental regulation of HSP26. Depression of HSP26 transcription may be the general mechanism of HSP26 induction in yeast cells. This regulatory scheme is very different from that described for the regulation of most other heat shock genes.
热休克蛋白26(Hsp26)是酿酒酵母中的一种小分子热休克蛋白,它会在热应激和其他类型的应激反应中积累。在正常发育过程中,当细胞进入稳定期生长或开始形成孢子时,它也会积累(S. Kurtz、J. Rossi、L. Petko和S. Lindquist,《科学》231:1154 - 1157,1986年)。对缺失和插入突变的分析表明,转录调控在调节Hsp26表达中起关键作用。研究发现Hsp26启动子很复杂,似乎包含抑制元件和激活元件。几个上游缺失突变导致Hsp26的强组成型表达。此外,Hsp26基因的上游序列抑制了异源热休克基因的组成型表达。我们认为,基础抑制和热诱导的转录抑制在调节Hsp26表达中起主要作用。我们分析的重组构建体中,没有一个能将负责热休克调节的顺式调控序列与负责Hsp26发育调控的序列分开。Hsp26转录的抑制可能是酵母细胞中Hsp26诱导的普遍机制。这种调控机制与大多数其他热休克基因的调控机制截然不同。