Delaney J M
Department of Microbiology and Immunology, College of Medicine, University of Arizona, Tucson 85724.
J Gen Microbiol. 1990 Oct;136(10):2113-8. doi: 10.1099/00221287-136-10-2113.
Thermotolerance in Escherichia coli is induced by exposing cells to a brief heat shock (42 degrees C for 15 min). This results in resistance to the lethal effect of exposure to a higher temperature (50 degrees C). Mutants defective in the recA, uvrA and xthA genes are more sensitive to heat than the wild-type. However, after development of thermotolerance these mutants are like the wild-type in their heat sensitivity. This suggests that thermotolerance is an inducible response capable of protecting cells from the lethal effects of heat, independently of recA, uvrA and xthA. Thermotolerance does not develop in a dnaK mutant. In addition, the dnaK mutant is sensitive to heat and H2O2, but is resistant to UV irradiation. This implies that the E. coli heat-shock response includes a mechanism that protects cells from heat and H2O2, but not from UV.
通过将大肠杆菌细胞暴露于短暂的热休克（42摄氏度，15分钟）可诱导其耐热性。这会导致细胞对暴露于更高温度（50摄氏度）的致死效应产生抗性。recA、uvrA和xthA基因有缺陷的突变体比野生型对热更敏感。然而，在耐热性形成后，这些突变体在热敏感性方面与野生型相似。这表明耐热性是一种可诱导的反应，能够独立于recA、uvrA和xthA保护细胞免受热的致死效应。dnaK突变体不会形成耐热性。此外，dnaK突变体对热和过氧化氢敏感，但对紫外线辐射有抗性。这意味着大肠杆菌的热休克反应包括一种保护细胞免受热和过氧化氢影响，但不能免受紫外线影响的机制。
