When repair mechanisms fail to keep up: high UVB irradiance causes disproportionate accumulation of DNA lesions

ABSTRACT Accumulation of unrepaired DNA lesions is a key mechanistic driver of mortality in organisms exposed to elevated ultraviolet-B radiation (UVBR). Recent research has found that high irradiance UVBR causes disproportionate mortality in larvae of a UV-sensitive amphibian (Limnodynastes peronii) compared with an equivalent dose of low irradiance UVBR. Here, we aimed to determine whether this irradiance-dependent effect is also reflected in the DNA damage profile of L. peronii larvae. Under laboratory conditions, we exposed larvae to one of two different UVBR irradiances over 2 days, keeping the daily dose equal by adjusting exposure duration. Larvae were sampled at set time points throughout experimental exposures for quantification of cyclobutane pyrimidine dimer (CPD) concentration. Larvae were highly susceptible to UVBR-induced CPD formation and had low rates of DNA repair, resulting in a carryover of DNA damage into the following day. Consequently, CPD concentrations accumulated to a higher level during the second day of exposure, an effect that was exacerbated by high irradiance exposure. Larvae exposed to high irradiance UVBR accumulated CPD lesions almost 3 times faster than larvae exposed at half the irradiance, causing a 47% increase in CPD concentration across sampling time points. These results demonstrate the capacity for high irradiance exposure to exacerbate UVBR-induced genomic instability, which may explain the irradiance-dependent mortality observed in this species. Given the conserved nature of DNA repair mechanisms across taxa, these findings have implications for other aquatic organisms with a larval life stage, including fish and coral, that are facing increasing UVBR levels owing to climate change.