Lage C, Menezes S
Departamento de Radiobiologia, Universidade Federal do Rio de Janeiro, Brazil.
J Photochem Photobiol B. 1994 Feb;22(2):157-64. doi: 10.1016/1011-1344(93)06966-7.
Heat-shock-induced resistance to far-UV (FUV) radiation was studied in Escherichia coli. The induction of FUV resistance was shown to be dependent on the products of the genes uvrA and polA in bacteria irradiated at 254 nm. Heat shock increased the resistance to 280 nm radiation in a uvrA6 recA13 mutant. Heat shock lowered the mutation frequency (reversion to tryptophan proficiency) in wild-type or uvrA strains irradiated at 254 nm. When these strains were irradiated at 280 nm, heat shock did not interfere with the mutation frequency in the wild-type strain, but greatly enhanced mutations in the uvrA mutant. After heat-shock treatment, the wild-type strain irradiated at 254 nm showed increased DNA degradation, indicating enhanced repair activity. However, heat shock did not stimulate SOS repair triggered by FUV. An increased survival of bacteriophages irradiated with FUV and inoculated into heat-shock-treated bacteria was not detected. The possibility that heat shock enhances excision repair activity in a wavelength-dependent manner is discussed.
对大肠杆菌中热休克诱导的抗远紫外线（FUV）辐射能力进行了研究。结果表明，在254nm波长下照射的细菌中，FUV抗性的诱导依赖于uvrA和polA基因的产物。热休克增加了uvrA6 recA13突变体对280nm辐射的抗性。热休克降低了在254nm波长下照射的野生型或uvrA菌株中的突变频率（回复到色氨酸原养型）。当这些菌株在280nm波长下照射时，热休克不影响野生型菌株中的突变频率，但极大地增强了uvrA突变体中的突变。热休克处理后，在254nm波长下照射的野生型菌株显示出DNA降解增加，表明修复活性增强。然而，热休克并未刺激由FUV触发的SOS修复。未检测到用FUV照射并接种到热休克处理过的细菌中的噬菌体存活率增加。讨论了热休克以波长依赖方式增强切除修复活性的可能性。
