Cold-induced skin darkening does not protect amphibian larvae from UV-associated DNA damage

Abstract

AbstractMany amphibian declines are correlated with increasing levels of ultraviolet radiation (UVR). While disease is often implicated in declines, environmental factors such as temperature and UVR play an important role in disease epidemiology.The mutagenic effects of UVR exposure on amphibians are worse at low temperatures. Amphibians from cold environments may be more susceptible to increasing UVR. However, larvae of some species demonstrate cold acclimation, reducing UV-induced DNA damage at low temperatures. Understanding of the mechanisms underpinning this response is lacking.We rearedLimnodynastes peroniilarvae in cool (15°C) or warm (25°C) waters before acutely exposing them to 1.5 h of high intensity (80 μW cm-2) UVBR. We measured the colour of larvae and mRNA levels of a DNA repair enzyme. We reared larvae at 25°C in black or white containers to elicit a skin colour response, and then measured DNA damage levels in the skin and remaining carcass following UVBR exposure.Cold acclimated larvae were darker and displayed lower levels of DNA damage than warm-acclimated larvae. There was no difference in CPD-photolyase mRNA levels between cold- and warm-acclimated larvae. Skin darkening in larvae did not reduce larval accumulation of DNA damage following UVR exposure.Our results showed that skin darkening alone does not explain cold-induced reductions in UV-associated DNA damage inL. peroniilarvae. Beneficial cold-acclimation is more likely underpinned by increased CPD-photolyase abundance and/or increased photolyase activity at low temperatures.Research HighlightsL. peroniiilarvae darken when exposed to cold temperaturesDarker larvae were not protected from the effects of UV on DNA damageCold acclimation of larvae when exposed to UV is likely driven by DNA repair enzymes not melanin