Biology subjects

Cramp, R.

Publications and source records attributed to Cramp, R..

3 recordsLinked to original sources

bioRxiv2023

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

O_LIMany 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. C_LIO_LIThe 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. C_LIO_LIWe reared Limnodynastes peronii larvae in cool (15{degrees}C) or warm (25{degrees}C) waters before acutely exposing them to 1.5 h of high intensity (80 W cm-2) UVBR. We measured the colour of larvae and mRNA levels of a DNA repair enzyme. We reared larvae at 25{degrees}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. C_LIO_LICold 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. C_LIO_LIOur results showed that skin darkening alone does not explain cold-induced reductions in UV-associated DNA damage in L. peronii larvae. Beneficial cold-acclimation is more likely underpinned by increased CPD-photolyase abundance and/or increased photolyase activity at low temperatures. C_LI Research HighlightsO_LIL. peroniii larvae darken when exposed to cold temperatures C_LIO_LIDarker larvae were not protected from the effects of UV on DNA damage C_LIO_LICold acclimation of larvae when exposed to UV is likely driven by DNA repair enzymes not melanin C_LI

molecular biology↗

bioRxiv2023

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.

zoology↗

bioRxiv2022

Temperature causes species-specific responses to UV-induced DNA damage in amphibian larvae

Anthropogenic ozone depletion has led to a 2-5% increase in ultraviolet B radiation (UVBR) levels reaching the earths surface. Exposure to UVBR causes harmful DNA damage in amphibians, but this is minimized by DNA repair enzymes such as thermally sensitive CPD-photolyase, with cool temperatures slowing repair rates. It is unknown whether amphibian species differ in the repair response to a given dose of UVBR across temperatures. We reared larvae of three species (Limnodynastes peronii, Limnodynastes tasmaniensis, and Platyplectrum ornatum) at 25{degrees}C and acutely exposed them to 80 W cm-2 UVBR for 2 h at either 20{degrees}C or 30{degrees}C. UVBR-mediated DNA damage was measured as larvae repaired damage in photoreactive light at their exposure temperatures. Cool temperatures increased DNA damage in all two species and slowed DNA repair rate in P. ornatum. The magnitude of DNA damage incurred from UVBR was species-specific. P. ornatum had the lowest CPDs and DNA repair rates, and the depressive effects of low temperature on photorepair were greater in L. tasmaniensis. Considering the susceptibility of most aquatic organisms to UVBR, this research highlighted a need to consider the complexity of species-specific physiology when forecasting the influence of changing UVBR and temperature in aquatic ecosystems.

molecular biology↗