SIGMA-32 SYNTHESIS CAN REGULATE THE SYNTHESIS OF HEAT-SHOCK PROTEINS IN ESCHERICHIA-COLI
SIGMA-32 SYNTHESIS CAN REGULATE THE SYNTHESIS OF HEAT-SHOCK PROTEINS IN ESCHERICHIA-COLI
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DOI：
10.1101/gad.1.2.179
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发表时间：
1987-04-01
影响因子：
10.5
通讯作者：
GROSS, CA
中科院分区：
文献类型：
--
作者：
GROSSMAN, AD;STRAUS, DB;GROSS, CA
大肠杆菌rpoH（htpR）基因产物σ 32是热激基因的正常表达和热激反应所需的。我们提出的实验表明σ 32在控制热激响应中的直接作用。热休克蛋白合成的诱导和下降都可以通过改变σ 32的合成速率来控制。具体而言，我们表明：（1）σ 32是不稳定的蛋白质，以大约4分钟的半衰期降解;（2）通过诱导Plac或Ptac-rpoH融合体的表达来增加σ 32的合成速率足以增加热休克蛋白的合成速率;（3）在热休克反应的关闭期，σ 32的合成在转录后被抑制，并且dnaK 756突变导致关闭期的缺陷，防止σ 32合成的转录后抑制。这些结果作为理解DnaK在热休克反应中的作用、σ 32合成的调节以及σ 32在控制热休克基因转录中的作用的基础。
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.