Mitchel R E, Morrison D P
Radiat Res. 1984 Aug;99(2):383-93.
Yeast, as well as higher eukaryotes, are induced to increase thermal resistance (thermotolerance) by prior exposure to a heat stress. Prior exposure to an acute dose of either 60Co gamma or 254-nm ultraviolet radiation, at sublethal or fractionally lethal doses, is shown to cause a marked increase in the resistance of Saccharomyces cerevisiae to killing by heat. Following a radiation exposure, thermal resistance increased with time during incubation in nutrient medium, and the degree of resistance reached was proportional to the dose received. Partial induction by radiation followed by maximum induction by heat did not produce an additive response when compared to a maximum induction by heat alone, suggesting that the same process was induced by both heat and radiation. Irradiation with 254-nm uv light followed by an immediate, partial photoreversal of the pyrimidine dimers with long-wavelength uv light resulted in a reduced level of resistance compared to cells not exposed to the photoreversal light, indicating that the cells specifically recognized pyrimidine dimers as a signal to increase their thermal resistance. Exposure to 254-nm uv or ionizing radiation induced thermal resistance in mutants defective in either excision repair (rad3, uv-sensitive) or recombinational repair (rad52, gamma-sensitive), suggesting that recognition and repair of DNA damage by these systems are not a part of the signal which initiates an increase in resistance to heat. The amount of induction, per unit dose, was greater in the DNA repair-deficient mutants than in the wild-type cells, suggesting that an increase in the length of time during which damage remains in the DNA results in an increase in the effectiveness of the induction. These data indicate that types of DNA damage as diverse as those produced by ionizing radiation and by ultraviolet light are recognized as a signal by the yeast cell to increase its thermal resistance. It is therefore suggested that heat-induced alterations in DNA or in DNA-dependent chromosomal organization may be the signal for heat induction of thermotolerance in this and other eukaryotes.
酵母以及高等真核生物，会通过预先暴露于热应激而被诱导提高热抗性（耐热性）。研究表明，预先暴露于亚致死剂量或部分致死剂量的急性剂量的60Coγ射线或254纳米紫外线辐射，会使酿酒酵母对热杀伤的抗性显著增加。辐射暴露后，在营养培养基中培养期间热抗性随时间增加，且达到的抗性程度与所接受的剂量成正比。与单独由热进行最大诱导相比，辐射进行部分诱导后再由热进行最大诱导并未产生累加反应，这表明热和辐射诱导的是相同的过程。用254纳米紫外线照射后，立即用长波长紫外线对嘧啶二聚体进行部分光逆转，与未暴露于光逆转光的细胞相比，抗性水平降低，这表明细胞将嘧啶二聚体特异性识别为增加其热抗性的信号。暴露于254纳米紫外线或电离辐射会在切除修复缺陷（rad3，对紫外线敏感）或重组修复缺陷（rad52，对γ射线敏感）的突变体中诱导热抗性，这表明这些系统对DNA损伤的识别和修复并非启动热抗性增加信号的一部分。每单位剂量的诱导量在DNA修复缺陷突变体中比在野生型细胞中更大，这表明DNA中损伤留存时间的增加会导致诱导效果增强。这些数据表明，酵母细胞将电离辐射和紫外线产生的多种类型的DNA损伤识别为增加其热抗性的信号。因此有人提出，DNA或依赖DNA的染色体组织中的热诱导变化可能是该生物及其他真核生物中热诱导耐热性的信号。
