Thermal compensation reduces DNA damage in UV-exposed amphibian larvae: implications for high latitudinal and altitudinal species

1. Increases in ultraviolet radiation (UVR) correlate spatially and temporally with global amphibian population declines and interact with other stressors such as disease and temperature. Declines have largely occurred in high-altitude areas associated with greater UVR and cooler temperatures. 2. UVR is a powerful mutagenic harming organisms largely by damaging DNA. When acutely exposed to UVR at cool temperatures, amphibian larvae have increased levels of DNA damage. Amphibians may be able to compensate for the depressive effects of temperature on DNA damage through thermal acclimatisation, but it is unknown whether they or other ectotherms have this capacity. 3. We reared striped marsh frog larvae (Limnodynastes peronii) in warm (25{degrees}C) and cool (15{degrees}C) temperatures under either a low or moderate daily dose of UVR (10 and 40 {micro}W cm-2 UV-B for 1 h at midday, respectively) for 18-20 days and then measured immediate DNA damage resulting from an acute high UVR dose (80 {micro}W cm-2 UV-B for 1.5 h) at a range of test temperatures (10, 15, 20, 25, and 30{degrees}C). 4. Larvae acclimated to 15{degrees}C and exposed to UVR at 15{degrees}C completely compensated UVR-induced DNA damage compared with 25{degrees}C acclimated larvae exposed to UVR at 25{degrees}C. Additionally, warm-acclimated larvae had higher CPDs than cold-acclimated larvae across test temperatures, which indicated a cost of living in warmer temperatures. In contrast, larvae reared under chronic elevated UVR levels showed no evidence of UVR acclimation resulting in lower DNA damage following an acute high UVR exposure. 5. Our finding that thermal acclimation in L. peronii larvae compensated UVR-induced DNA damage at low temperatures suggested that aquatic ectotherms living in cool temperatures may be more resilient to high UVR than previously realised. 6. We suggested individuals or species with less capacity for thermal acclimation of DNA repair mechanisms may be more at risk if exposed to changing thermal and UVR exposure regimes but cautioned that thermal acclimation of DNA repair mechanisms may not always be beneficial.