Xue Y, Nicholson W L
Department of Microbiology and Immunology, University of North Texas Health Science Center, Fort Worth 76107, USA.
Appl Environ Microbiol. 1996 Jul;62(7):2221-7. doi: 10.1128/aem.62.7.2221-2227.1996.
Bacterial endospores are 1 to 2 orders of magnitude more resistant to 254-nm UV (UV-C) radiation than are exponentially growing cells of the same strain. This high UV resistance is due to two related phenomena: (i) DNA of dormant spores irradiated with 254-nm UV accumulates mainly a unique thymine dimer called the spore photoproduct (SP), and (ii) SP is corrected during spore germination by two major DNA repair pathways, nucleotide excision repair (NER) and an SP-specific enzyme called SP lyase. To date, it has been assumed that these two factors also account for resistance of bacterial spores to solar UV in the environment, despite the fact that sunlight at the Earth's surface consists of UV-B, UV-A, visible, and infrared wavelengths of approximately 290 nm and longer. To test this assumption, isogenic strains of Bacillus subtilis lacking either the NER or SP lyase DNA repair pathway were assayed for their relative resistance to radiation at a number of UV wavelengths, including UV-C (254 nm), UV-B (290 to 320 nm), full-spectrum sunlight, and sunlight from which the UV-B portion had been removed. For purposes of direct comparison, spore UV resistance levels were determined with respect to a calibrated biological dosimeter consisting of a mixture of wild-type spores and spores lacking both DNA repair systems. It was observed that the relative contributions of the two pathways to spore UV resistance change depending on the UV wavelengths used in a manner suggesting that spores irradiated with light at environmentally relevant UV wavelengths may accumulate significant amounts of one or more DNA photoproducts in addition to SP. Furthermore, it was noted that upon exposure to increasing wavelengths, wild-type spores decreased in their UV resistance from 33-fold (UV-C) to 12-fold (UV-B plus UV-A sunlight) to 6-fold (UV-A sunlight alone) more resistant than mutants lacking both DNA repair systems, suggesting that at increasing solar UV wavelengths, spores are inactivated either by DNA damage not reparable by the NER or SP lyase system, damage caused to photosensitive molecules other than DNA, or both.
细菌芽孢对254纳米紫外线（UV-C）辐射的抗性比同一菌株处于指数生长期的细胞高1至2个数量级。这种高抗紫外线性是由于两个相关现象：（i）用254纳米紫外线照射的休眠芽孢的DNA主要积累一种独特的胸腺嘧啶二聚体，称为芽孢光产物（SP），以及（ii）在芽孢萌发过程中，SP通过两种主要的DNA修复途径，即核苷酸切除修复（NER）和一种称为SP裂解酶的SP特异性酶进行校正。迄今为止，尽管地球表面的阳光由紫外线B、紫外线A、可见光和波长约为290纳米及更长的红外线组成，但人们一直认为这两个因素也解释了细菌芽孢在环境中对太阳紫外线的抗性。为了验证这一假设，对缺乏NER或SP裂解酶DNA修复途径的枯草芽孢杆菌同基因菌株进行了检测，以确定它们对多种紫外线波长辐射的相对抗性，包括UV-C（254纳米）、UV-B（290至320纳米）、全光谱阳光以及去除了UV-B部分的阳光。为了进行直接比较，相对于由野生型芽孢和缺乏两种DNA修复系统的芽孢混合组成的校准生物剂量计，测定了芽孢的抗紫外水平。观察到这两种途径对芽孢抗紫外线性的相对贡献会根据所使用的紫外线波长而变化，这表明用环境相关紫外线波长的光照射的芽孢除了SP之外，可能还会积累大量的一种或多种DNA光产物。此外，还注意到随着照射波长的增加，野生型芽孢的抗紫外能力从比缺乏两种DNA修复系统的突变体高33倍（UV-C）降至12倍（UV-B加UV-A阳光）再降至6倍（仅UV-A阳光），这表明随着太阳紫外线波长的增加，芽孢要么被NER或SP裂解酶系统无法修复的DNA损伤、对DNA以外的光敏分子造成的损伤，要么被这两种损伤共同灭活。
