1. The interaction between UV-B and temperature can modify the effects of climate variability on animal function because UV-B and increasing temperatures may increase reactive oxygen species (ROS) production and thereby impair animal performance. However, antioxidant enzyme activities are also increased at higher temperatures, which could counteract negative effects of increased ROS. Conversely, UV-B exposure at lower temperature can exacerbate the effects of ROS because of lower antioxidant enzyme activities. 2. Phenotypes can be plastic to compensate for potentially negative environmental effects. Plasticity may be induced by conditions experienced during pre-or early post-zygotic development, and it may occur reversibly within adult organisms (acclimation). Developmental plasticity and acclimation may interact to determine phenotypes in variable environments.3. Here, we tested the hypothesis that increased antioxidant enzyme activities are insufficient to alleviate the interactive effects of UV-B and increased temperature on mosquitofish (Gambusia holbrooki). Additionally, we tested whether developmental conditions influenced the capacity for acclimation to UV-B and temperature so that cohorts born in summer at high UV-B and temperature conditions are better able to compensate for ROS damage compared to cohorts born in winter. 4. We exposed mosquitofish to UV-B and control (no-UV-B) at different acclimation temperatures (18, 28 and 32°C), and measured responses acutely at 18, 28 and 32°C in a fully factorial design. In fish born in summer, UV-B had significant negative effects on swimming performance and resting metabolic rate at both low (18°C) and high (32°C) acclimation temperatures, which were accompanied by higher ROS-induced damage. At their average temperature experienced naturally (28°C), fish born in summer were not affected by UV-B and showed lower damage and higher antioxidant enzyme activities compared to the other acclimation temperatures. In contrast, swimming performance of winter-caught fish was negatively affected by UV-B at all acclimation temperatures, which was paralleled by higher ROS-induced damage and antioxidant enzyme activities that did not acclimate. However, metabolic scope was not reduced by UV-B or temperature in any of the cohorts. 5. Our results showed that developmental conditions modify the capacity for acclimation later in life, and that the interaction between developmental and acclimation conditions can increase the resilience of animals to environmental variability. These results have important implications for understanding the evolution of acclimation, and for predictions of how climate change affects animal performance.

Ultraviolet B radiation (UV-B) can reduce swimming performance by increasing reactive oxygen species (ROS) formation. High concentrations of ROS can damage mitochondria, resulting in reduced ATP production. ROS can also damage muscle proteins, thereby leading to impaired muscle contractile function. We have shown previously that UV-B exposure reduces locomotor performance in mosquitofish (Gambusia holbrooki) without affecting metabolic scope. Our aim was therefore to test whether UV-B influences swimming performance of mosquitofish by ROS-induced damage to muscle proteins without affecting mitochondrial function. In a fully factorial design, we exposed mosquitofish to UV-B and no-UV-B controls in combination with exposure to N-acetylcysteine (NAC) plus no-NAC controls. We used NAC, a precursor of glutathione, as an antioxidant to test whether any effects of UV-B on swimming performance were at least partly due to UV-B-induced ROS. UV-B significantly reduced critical sustained swimming performance and tail beat frequencies, and it increased ROS-induced damage (protein carbonyl concentrations and lipid peroxidation) in muscle. However, UV-B did not affect the activity of sarco-endoplasmic reticulum ATPase (SERCA), an enzyme associated with muscle calcium cycling and muscle relaxation. UV-B did not affect ADP phosphorylation (state 3) rates of mitochondrial respiration, and it did not alter the amount of ATP produced per atom of oxygen consumed (P:O ratio). However, UV-B reduced the mitochondrial respiratory control ratio. Under UV-B exposure, fish treated with NAC showed greater swimming performance and tail beat frequencies, higher glutathione concentrations, and lower protein carbonyl concentrations and lipid peroxidation than untreated fish. Tail beat amplitude was not affected by any treatment. Our results showed, firstly, that the effects of UV-B on locomotor performance were mediated by ROS and, secondly, that reduced swimming performance was not caused by impaired mitochondrial ATP production. Instead, reduced tail beat frequencies indicate that muscle of UV-B exposed fish were slower, which was likely to have been caused by slower contraction rates, because SERCA activities remained unaffected.

Temperature and ultraviolet B (UV-B) interact in causing cellular damage and impairing locomotor performance. Here, we test the hypothesis that movement and thermal selection of zebrafish (Danio rerio) change in the presence of UV-B, and in particular, that fish which were chronically exposed to UV-B avoid high and low temperature extremes to maximize activities of antioxidant enzymes. Fish chronically (two to three weeks) exposed to UV-B had increased reactive oxygen species (ROS)-induced damage to proteins and membranes, and reduced swimming performance at high (more than 268C) temperatures. In an open field arena with a thermal gradient, chronically exposed fish avoided high and low temperature extremes compared with control fish. Additionally, both control and chronically exposed fish showed slower voluntary swimming speeds in the presence of UV-B. We suggest that in the presence of UV-B fish may reduce muscular activity to minimize intrinsic ROS production. Our data show that the interaction between UV-B and temperature determines movement and microhabitat selection of fish, which is therefore of ecological importance particularly in anthropogenically modified environments.

Summary The environment experienced by parents can alter offspring phenotypes. Such developmental plasticity is beneficial when it optimises offspring responses to their prevailing environment. Plasticity may be detrimental, however, if there is a mismatch between parental and offspring environments, although reversible acclimation within individuals could counteract a developmental mismatch. UV‐B radiation damages cells directly and by increasing reactive oxygen species (ROS) formation. There are indications that the developmental environment can influence ROS defences, which could enhance performance and fitness. In addition, animals exposed to UV‐B can acclimate to increase their antioxidant defences and thereby reduce ROS‐induced damage. Our aim was to test experimentally whether there are transgenerational effects of UV‐B exposure. We tested the hypothesis that parental exposure to UV‐B modulates offspring ROS defence mechanisms to reduce the negative effects of UV‐B in offspring. In a fully factorial experiment, we show that exposing guppies (Poecilia reticulata) to UV‐B increased the resilience of their offspring to the negative effects of UV‐B. When exposed to UV‐B, offspring from parents also exposed to UV‐B had significantly greater sustained swimming performance compared to controls. Higher swimming performance was paralleled by increased catalase activity and glutathione concentrations, and reduced ROS‐induced damage to membranes and proteins. There was no effect of parental exposure to UV‐B on offspring superoxide dismutase activity, resting and active metabolic rates or offspring size. However, parental exposure to UV‐B increased damage to proteins and infection rates by white spot fungus in control (no UV‐B) offspring. Our results showed that UV‐B acts as a signal that can induce developmental modification of phenotypes. Transgenerational matching of offspring phenotypes is likely to have a fitness advantage in environments exposed to UV‐B. However, the trade‐off between the beneficial effects of parental UV‐B exposure on offspring performance when exposed to UV‐B, and the increased susceptibility to infection and protein damage when offspring are not exposed to UV‐B can be important in determining the resilience of populations in variable and modified environments. A http://onlinelibrary.wiley.com/doi/10.1111/1365-2435.12817/suppinfo is available for this article.

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