DNAK, DNAJ, AND GRPE HEAT-SHOCK PROTEINS NEGATIVELY REGULATE HEAT-SHOCK GENE-EXPRESSION BY CONTROLLING THE SYNTHESIS AND STABILITY OF SIGMA-32
DNAK, DNAJ, AND GRPE HEAT-SHOCK PROTEINS NEGATIVELY REGULATE HEAT-SHOCK GENE-EXPRESSION BY CONTROLLING THE SYNTHESIS AND STABILITY OF SIGMA-32
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DOI：
10.1101/gad.4.12a.2202
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发表时间：
1990-12-01
影响因子：
10.5
通讯作者：
GROSS, CA
中科院分区：
文献类型：
--
作者：
STRAUS, D;WALTER, W;GROSS, CA
大肠杆菌DNAK热休克蛋白是大肠杆菌热休克基因表达的负调控因子。我们报道了另外两个热休克蛋白，DNAJ和GRPE，也参与了热休克基因表达的负调控。携带缺陷dna K、dna J或GRPE等位基因的菌株在低温下可以促进心脏休克蛋白的合成，并且在转变到高温后无法关闭热休克反应。这些调节缺陷是由于失去了对α32合成和稳定性的正常控制，β32是热休克基因表达所需的交替RNA聚合酶α因子。我们的结论是，DNAK、DNAJ和GRPE调节α的浓度。32我们认为热休克蛋白的合成是由一个将热休克蛋白的功能与α32的浓度联系起来的动态平衡机制控制的。
The Escherichia coli DnaK heat shock protein has been identified previously as a negative regulator of E. coli heat shock gene expression. We report that two other heat shock proteins, DnaJ and GrpE, are also involved in the negative regulation of heat shock gene expression. Strains carrying defective dnaK, dnaJ, or grpE alleles have enhanced synthesis of heart shock protein at low temperature and fail to shut off the heat shock response after shift to high temperature. These regulatory defects are due to the loss of normal control over the synthesis and stability of .sigma.32, the alternate RNA polymerase .sigma.-factor required for heat shock gene expression. We conclude that DnaK, DnaJ, and GrpE regulate the concentration of .sigma.32 WE suggest that the synthesis of heat shock proteins is controlled by a homeostatic mechanism linking the function of heat shock proteins to the concentration of .sigma.32.