Ries G, Buchholz G, Frohnmeyer H, Hohn B
Friedrich Miescher-Institut, Post Office Box 2543, CH-4002 Basel, Switzerland.
Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13425-9. doi: 10.1073/pnas.230251897.
Plants are continuously subjected to UV-B radiation (UV-B; 280-320 nm) as a component of sunlight causing damage to the genome. For elimination of DNA damage, a set of repair mechanisms, mainly photoreactivation, excision, and recombination repair, has evolved. Whereas photoreactivation and excision repair have been intensely studied during the last few years, recombination repair, its regulation, and its interrelationship with photoreactivation in response to UV-B-induced DNA damage is still poorly understood. In this study, we analyzed somatic homologous recombination in a transgenic Arabidopsis line carrying a beta-glucuronidase gene as a recombination marker and in offsprings of crosses of this line with a photolyase deficient uvr2-1 mutant. UV-B radiation stimulated recombination frequencies in a dose-dependent manner correlating linearly with cyclobutane pyrimidine dimer (CPD) levels. Genetic deficiency for CPD-specific photoreactivation resulted in a drastic increase of recombination events, indicating that homologous recombination might be directly involved in eliminating CPD damage. UV-B irradiation stimulated recombination mainly in the presence of photosynthetic active radiation (400-700 nm) irrespective of photolyase activities. Our results suggest that UV-B-induced recombination processes may depend on energy supply derived from photosynthesis.
植物作为阳光的一部分，持续受到UV - B辐射（280 - 320纳米），这种辐射会对基因组造成损害。为了消除DNA损伤，一套修复机制已经进化出来，主要包括光复活、切除和重组修复。尽管在过去几年中对光复活和切除修复进行了深入研究，但对于重组修复、其调控以及它与响应UV - B诱导的DNA损伤时的光复活之间的相互关系仍知之甚少。在本研究中，我们分析了携带β - 葡萄糖醛酸酶基因作为重组标记的转基因拟南芥品系以及该品系与光裂合酶缺陷型uvr2 - 1突变体杂交后代中的体细胞同源重组。UV - B辐射以剂量依赖的方式刺激重组频率，该频率与环丁烷嘧啶二聚体（CPD）水平呈线性相关。CPD特异性光复活的遗传缺陷导致重组事件急剧增加，这表明同源重组可能直接参与消除CPD损伤。无论光裂合酶活性如何，UV - B照射主要在光合有效辐射（400 - 700纳米）存在的情况下刺激重组。我们的结果表明，UV - B诱导的重组过程可能依赖于光合作用产生的能量供应。
