Grossman A D, Straus D B, Walter W A, Gross C A
Department of Bacteriology, University of Wisconsin-Madison 53706.
Genes Dev. 1987 Apr;1(2):179-84. doi: 10.1101/gad.1.2.179.
The Escherichia coli rpoH (htpR) gene product, sigma 32, is required for the normal expression of heat shock genes and for the heat shock response. We present experiments indicating a direct role for sigma 32 in controlling the heat shock response. Both the induction and decline in the synthesis of heat shock proteins can be controlled by changes in the rate of synthesis of sigma 32. Specifically, we show that: (1) sigma 32 is an unstable protein, degraded with a half-life of approximately 4 min; (2) increasing the rate of synthesis of sigma 32, by inducing expression from a Plac or Ptac-rpoH fusion, is sufficient to increase the rate of synthesis of heat shock proteins; (3) during the shut-off phase of the heat shock response synthesis of sigma 32 is repressed post-transcriptionally, and the dnaK756 mutation, which causes a defect in the shut-off phase, prevents the post-transcriptional repression of synthesis of sigma 32. These results serve as a basis for understanding the role of DnaK in the heat shock response, the regulation of sigma 32 synthesis, and the role of sigma 32 in controlling transcription of heat shock genes.
大肠杆菌rpoH（htpR）基因产物σ32，是热休克基因正常表达和热休克反应所必需的。我们进行的实验表明，σ32在控制热休克反应中起直接作用。热休克蛋白合成的诱导和下降都可由σ32合成速率的变化来控制。具体而言，我们发现：（1）σ32是一种不稳定蛋白，半衰期约为4分钟；（2）通过诱导Plac或Ptac-rpoH融合体的表达来提高σ32的合成速率，足以提高热休克蛋白的合成速率；（3）在热休克反应的关闭阶段，σ32的合成在转录后受到抑制，而导致关闭阶段出现缺陷的dnaK756突变会阻止σ32合成的转录后抑制。这些结果为理解DnaK在热休克反应中的作用、σ32合成的调控以及σ32在控制热休克基因转录中的作用奠定了基础。
