Craig E. Franklin

Metabolic depression occurs across a diverse array of invertebrate and vertebrate animals during aestivation (summer dormancy). Some aestivating vertebrates form a protective cocoon of shed epidermal layers (amphibians) or dried mucus (lungfishes) which precludes activity, and their metabolic rates (0.14–0.44 of standard) are typically lower and more stable than for non-cocooning aestivators. Their transition to aestivation appears to be an intrinsic response to inactivity and adoption of the water-conserving posture rather than extrinsic environmental changes such as temperature or hypoxia. Physiological consequences include a transition from pulmo-cutaneous to primarily pulmonary gas exchange, with consequential changes in ventilation and circulation. Breathing rate increases, heart rate decreases, and there is likely a slight decrease in blood pO ₂ and a mild blood acidosis. Cocoon-forming frogs are an ideal model for mechanistic studies of intrinsic metabolic depression, but little progress has been made in resolving underlying molecular mechanisms. To date, ‘omics’ approaches have been largely restricted to genome-wide expression of a single tissue (gastrocnemius muscle) in just one Australian species ( Cyclorana alboguttata ). Future research should expand both taxonomic and physiological coverage by characterising additional metabolically important tissues such as liver, kidney, bladder and skin. It should also investigate multiple levels of biological organisation beyond mRNA, including genome size and structure, CpG methylation, histone acetylation, protein abundance and post-translational modifications, intracellular signalling cascades and metabolite profiles. Comparative analyses of the different dynamics of entry into and arousal from aestivation, as well as steady-state metabolic depression, will be informative regarding mechanisms for metabolic depression. Competing Interests: None of the authors have any competing interests.

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.

Relative to other subdisciplines of conservation science, conservation physiology remains somewhat nascent. Although there is a growing number of successes where physiological concepts, knowledge and tools have informed conservation decisions and management actions, there also remain a number of challenges. We argue that there is a set of misconceptions that serve as de facto barriers to realizing the full potential of conservation physiology as a mission-oriented area of scholarly inquiry and practice. However, we also suggest that those misconceptions can be easily dispelled. In this paper, we identify and dispel 10 ‘myths’ in conservation physiology: (i) conservation physiology subsumes other disciplines and has no unique goals; (ii) the toolbox is too invasive; (iii) tools are too specialized; (iv) the field relies too heavily on surrogates and captive studies; (v) physiological information cannot be scaled from the individual level to the population level; (vi) baseline (i.e. control) data are too sparse; (vii) conservation physiology is too speculative; (viii) managers do not care about physiology; (ix) conservation physiology cannot engage fundamental scientists; and (x) conservation physiology cannot solve conservation problems. Given that some of these misconceptions represent ongoing barriers, we also identify opportunities for further overcoming them. In particular, embracing co-production and engaging in effective knowledge exchange are fundamental to generating relevant and actionable knowledge. Similarly, we submit that the tension between fundamental and applied science is not inherently disruptive and ensures that there is a strong foundation for evidence-based decisions. This paper is intended to open the eyes and minds of ecologists, physiologists and end-users about what conservation physiology has to offer and how to realize those opportunities. Working collectively and collaboratively to achieve the common mission of conservation physiology will not only benefit conservation science but will also benefit biodiversity and society.

Ambient sunlight contains ultraviolet radiation (UVR), a potent genotoxic stressor, yet whether natural UVR induces DNA damage in free-living amphibian larvae remains unclear. We reared striped marsh frogs (Limnodynastes peronii) in outdoor mesocosms under low versus high ambient UVR treatments for 5 days and quantified cyclobutane pyrimidine dimers (CPDs) by ELISA. Measurable CPD levels were detected under both UVR exposures, providing direct evidence that natural sunlight induces DNA damage in amphibian larvae. Although mean CPD levels did not differ between treatments, quantile regression revealed higher levels of CPDs in both the lower (τ=0.05) and upper (τ=0.95) quantiles under high UVR. This pattern suggests that while average DNA damage levels were similar, subsets of individuals experienced disproportionately high CPD burdens under increased UVR. These results highlight the value of mesocosms as a tool to bridge laboratory and field contexts to evaluate the effects of UVR on aquatic fauna, particularly as UV environments shift with climate change.

Loss of structural habitat complexity associated with habitat degradation in marine systems may expose early life stages of fishes to harsh environmental conditions. Specifically, loss of coral cover means less suitable refuge is available for some reef fish species to lay their eggs, exposing them to pervasive stressors such as ultraviolet radiation (UVR). Here, using laboratory experiments, we exposed embryos of the clownfish Amphiprion ocellaris for 2 h daily to two UVR levels reflective of their depth at settlement; high UVR (280 µW m−2), reflective of shallow depths, and low UVR (80 µW m−2), reflective of deeper depths over their embryonic period, and then measured changes in mass, yolk sac volume, DNA damage, and survival. Despite being exposed to ecologically relevant levels of UV radiation, there was 100% mortality before hatching and inflated yolk sacs in both high and low UVR-treated animals. Exposure to UVR also resulted in DNA damage, albeit only in high UVR treatments. It is evident from our results that the protection that the reef can offer from UVR is critical for the survival of clownfish. Our results also underscore the need for future work to consider this often-neglected stressor and the role of adequate refuge for the healthy development of early-life stages of reef organisms.

Ultraviolet radiation (UVR) has a range of strong effects on freshwater ecosystems, and changing UVR is implicated in global amphibian declines. The link between UVR and amphibian declines is not well understood, largely due to limited understanding of actual UVR exposure regimes in freshwater ecosystems. Logistical challenges in measuring aquatic UVR regimes in situ have impeded progress, including the design of cost-effective radiometric monitoring tools and the measurement of UVR at ecologically relevant scales. We designed novel underwater UVR loggers and deployed them in southeast Queensland creeks to log near-continuous underwater ultraviolet index (UVI) for 11 days across four sampling events within the peak amphibian breeding season. We compared these data with solar modelling, dosimetric and handheld radiometric techniques. The dataset (2616 h from 39 UV sensors) revealed a highly heterogenous daily UVR microenvironment that showed capacity for harmful UVI exposures at both sites. Traditional cumulative or periodic UVR monitoring approaches often missed these acute high UVR exposures. Fine scale UVR data logging was proven to be a cost-effective approach for monitoring the UVR microenvironment in freshwater systems. While no single method can be considered universally optimal, our results highlight the advantages of continuous in situ UV monitoring, particularly for capturing short-duration ultraviolet fluctuations relevant to aquatic organisms.