Data from: Divergence in DNA photorepair efficiency among genotypes from contrasting UV radiation environments in nature

Populations of organisms routinely face abiotic selection pressures, and a central goal of evolutionary biology is to understand the mechanistic underpinnings of adaptive phenotypes. Ultraviolet radiation (UVR) is one of earth’s most pervasive environmental stressors, potentially damaging DNA in any organism exposed to solar radiation. We explored mechanisms underlying differential survival following UVR exposure in genotypes of the water flea Daphnia melanica derived from natural ponds of differing in UVR intensity. The UVR tolerance of a D. melanica genotype from a high-UVR habitat depended on the presence of visible and UV-A light wavelengths necessary for photoenzymatic repair of DNA damage, a repair pathway widely shared across the tree of life. We then measured the acquisition and repair of cyclobutane pyrimidine dimers, the primary form of UVR-caused DNA damage, in D. melanica DNA following experimental UVR exposure. We demonstrate that genotypes from high-UVR habitats repair DNA damage faster than genotypes from low-UVR habitats in the presence of visible and UV-A radiation necessary for photoenzymatic repair, but not in dark treatments. Because differences in repair rate only occurred in the presence of visible and UV-A radiation, we conclude that differing rates of DNA repair, and therefore differential UVR tolerance, are a consequence of variation in photoenzymatic repair efficiency. We then rule out a simple gene expression hypothesis for the molecular basis of differing repair efficiency, as expression of the CPD photolyase gene photorepair did not differ among D. melanica lineages, both in the presence and absence of UVR.

生物种群普遍面临非生物选择压力，进化生物学的核心目标之一是阐明适应性表型的机制基础。紫外线辐射（ultraviolet radiation，UVR）是地球分布最为广泛的环境胁迫因子之一，可对暴露于太阳辐射下的所有生物的DNA造成损伤。我们针对采自UVR强度各异的天然池塘的黑纹溞（Daphnia melanica）基因型，探究了其在UVR暴露后差异化存活的潜在机制。来自高UVR生境的黑纹溞基因型的UVR耐受性，取决于可见光与UV-A波长的存在——这类波长是DNA损伤光酶修复所必需的，而该修复通路广泛存在于整个生命之树中。随后，我们测定了实验性UVR暴露后，黑纹溞DNA中环丁烷嘧啶二聚体（cyclobutane pyrimidine dimers）的积累与修复情况——该物质是UVR引发的DNA损伤的主要形式。我们证实，在光酶修复所需的可见光与UV-A辐射存在的条件下，来自高UVR生境的基因型的DNA损伤修复速率显著快于来自低UVR生境的基因型；而在黑暗处理组中则无此差异。由于修复速率的差异仅在可见光与UV-A辐射存在时出现，我们推断，DNA修复速率的差异（进而导致UVR耐受性的差异）是光酶修复效率变异的结果。随后，我们排除了基于简单基因表达假说的修复效率差异分子机制：无论是否存在UVR，黑纹溞各谱系间的CPD光裂合酶基因的表达量均无显著差异。