Molecular and sensory mechanisms to mitigate sunlight-induced DNA damage in treefrog tadpoles

Abstract

The increased incidence of solar ultraviolet B (UVB) radiation has been proposed as an environmental stressor, which may help to explain the enigmatic decline of amphibian populations worldwide. Despite growing knowledge regarding the UV-induced biological effects in several amphibian models, little is known about the efficacy of DNA repair pathways. In addition, little attention has been given to the interplay between these molecular mechanisms with other physiological strategies that avoid the damage induced by sunlight. Here, DNA lesions induced by environmental doses of solar UVB and UVA radiation were detected in genomic DNA samples of treefrog tadpoles (Hypsiboas pulchellus) and their DNA repair activity was evaluated. These data were complemented by monitoring the induction of apoptosis in blood cells and tadpole survival. Furthermore, the tadpoles' ability to perceive and escape from UV wavelengths was evaluated as an additional strategy of photoprotection. The results show that tadpoles are very sensitive to UVB light, which could be explained by the slow DNA repair rates for both cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6,4) pyrimidone photoproducts (6,4PPs). However, they were resistant to UVA, probably as a result of the activation of photolyases during UVA irradiation. Surprisingly, a sensory mechanism that triggers their escape from UVB and UVA light avoids the generation of DNA damage and helps to maintain the genomic integrity. This work demonstrates the genotoxic impact of both UVB and UVA radiation on tadpoles and emphasizes the importance of the interplay between molecular and sensory mechanisms to minimize the damage caused by sunlight.

Cooler temperatures slow the repair of DNA damage in tadpoles exposed to ultraviolet radiation: Implications for amphibian declines at high altitude

“…Amphibians are affected by UVBR through its impacts on DNA and other biological molecules (Alton & Franklin, ; Bancroft et al, ; Blaustein & Kiesecker, ; Schuch, Dos Santos, et al, ; Schuch, Lipinski, et al, ). DNA damage occurs when UVBR energy is absorbed by DNA causing neighbouring pyrimidine bases on the same DNA strand to become covalently linked (Schuch, Garcia, Makita, & Menck, ).…”

Enhanced Phylogenetic Diversity of Anuran Communities: A Result of Species Loss in an Agricultural Environment

“…This may be due the large number of traits presented by each species and/or the high species number existing in many habitats which generates an incomplete knowledge of which species traits can actually be an influence to the ecosystem processes [21]. Among all vertebrates, the amphibians are the group with highest proportion of species threatened with extinction [22], due to habitat loss, fragmentation [23], and other related environmental stressors like enhanced UV radiation incidence [24,25] and canopy coverage loss [26]. Furthermore, the complexity on amphibian life cycle and the differences in life-history strategies between species and also their habitat associations generate a need for studies aiming to understand the true relationship between anthropogenic disturbance and the structure and organization of amphibian communities [7,8].…”

Early exposure to UV radiation causes telomere shortening and poorer condition later in life

“…UVBR also causes oxidative stress through the production of reactive oxygen species (ROS; Heck et al 2003; Kazerouni et al 2016), although ultraviolet-A radiation (UVAR; 315-400 nm) is more potent in this regard (Schuch et al 2017). Despite organisms having DNA repair mechanisms to remove UVBR-induced DNA damage (Sancar and Sancar 1988; Sancar and Tang 1993; Schuch et al, 2015b), even minor increases in UVBR irradiance may be sufficient to tip DNA damage rates beyond the capacity for repair, which can have detrimental downstream effects on organismal condition and survival (Blaustein et al 1994, Pandelova et al 2006, Schuch et al 2015b).…”