VanBogelen R A, Acton M A, Neidhardt F C
Department of Microbiology and Immunology, University of Michigan, Ann Arbor 48109-0620.
Genes Dev. 1987 Aug;1(6):525-31. doi: 10.1101/gad.1.6.525.
The addition of isopropyl thio-beta-D-galactoside (IPTG) to Escherichia coli cells containing multiple copies of the heat shock regulatory gene htpR (rpoH) under the control of an IPTG-inducible promoter (P-tac) induced 15 of the 17 polypeptides of the heat shock (HTP) regulon. The time course and magnitude of the induction closely resembled that caused by a shift to 42 degrees C. Nevertheless the two means of inducing the heat shock regulon differed in outcome. Cultures grown at 28 degrees C and induced by incubation at 42 degrees C for 15 min gave significant protection against a challenge temperature of 50 degrees C, but no protection was afforded by a 15-min IPTG treatment at 28 degrees C. It could be shown that there was no interference by IPTG with the development of thermotolerance at 42 degrees C. Also, treatment of a wild strain of E. coli with various toxic agents revealed no correlation between the development of thermotolerance and the induction of any subset of the heat shock proteins. Thermotolerance appears to develop by processes other than the htpR-dependent induction of heat shock proteins.
在含有多个拷贝的热休克调节基因htpR（rpoH）且受异丙基硫代-β-D-半乳糖苷（IPTG）诱导型启动子（P-tac）控制的大肠杆菌细胞中添加IPTG，可诱导热休克（HTP）调节子的17种多肽中的15种。诱导的时间进程和幅度与转移至42℃所引起的情况极为相似。然而，诱导热休克调节子的这两种方式在结果上有所不同。在28℃生长的培养物，经42℃孵育15分钟诱导后，对50℃的挑战温度有显著的保护作用，但在28℃进行15分钟的IPTG处理则没有提供保护。可以证明，IPTG不会干扰在42℃时耐热性的发展。此外，用各种有毒试剂处理大肠杆菌野生菌株表明，耐热性的发展与热休克蛋白任何亚组的诱导之间没有相关性。耐热性似乎是通过依赖htpR诱导热休克蛋白以外的过程发展而来的。
