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Wilson, R. W.

Publications and source records attributed to Wilson, R. W..

4 recordsLinked to original sources

Combining population genomics and transcriptomics to identify signatures of metal tolerance in brown trout inhabiting metal-polluted rivers

Industrial pollution is a major driver of ecosystem degradation, but it can also act as a driver of contemporary evolution. As a result of intense mining activity during the Industrial Revolution, several rivers across the southwest of England are polluted with high concentrations of metals. Despite the documented negative impacts of ongoing metal pollution, brown trout (Salmo trutta L.) survive and thrive in many of these metal-impacted rivers. We used population genomics, transcriptomics, and metal burdens to investigate the genomic and transcriptomic signatures of potential metal tolerance. RADseq analysis of six populations (originating from three metal-impacted and three control rivers) revealed strong genetic substructuring between impacted and control populations. We identified selection signatures at 122 loci, including genes related to metal homeostasis and oxidative stress. Trout sampled from metal-impacted rivers exhibited significantly higher tissue concentrations of cadmium, copper, nickel, and zinc, which remained elevated after 11 days in metal-free water. After depuration, we used RNAseq to quantify gene expression differences between metal-impacted and control trout, identifying 2,042 differentially expressed genes (DEGs) in the gill, and 311 DEGs in the liver. Transcriptomic signatures in the gill were enriched for genes involved in ion transport processes, metal homeostasis, oxidative stress, hypoxia and response to xenobiotics. Our findings reveal shared genomic and transcriptomic pathways involved in detoxification, oxidative stress responses, and ion regulation. Overall, our results demonstrate the diverse effects of metal pollution in shaping both neutral and adaptive genetic variation, whilst also highlighting the potential role of constitutive gene expression in promoting metal tolerance.

evolutionary biology↗

Fish Blood Response to Ash-Induced Environmental Alkalinization, and their Implications to Wildfire-Scarred Watersheds

Changes in land use, warming climate and increased drought have amplified wildfire frequency and magnitude globally. Ash mixing into aquatic systems after wildfires rapidly increases water pH, creating an additional threat to wildlife, especially species that are already threatened, endangered and/or migratory. Here, Chinook salmon (Oncorhynchus tshawytscha) yearlings acclimated to 15 or 20{degrees}C were exposed to an environmentally relevant concentration of ash (0.25% w/v) which caused water pH to rapidly rise from [~]8.1 to [~]9.2. Mortalities occurred within the first 12 hours, and was higher at the higher temperature (33 versus 20 %). The greatest differences in blood chemistry between the two temperatures were dramatically greater ([~]7.5-fold) and very rapid (within 1 hour) spikes in both plasma total ammonia (to [~]1200 {micro}M) and lactate (to [~]6 mM) in warm-acclimated salmon, whereas cold-acclimated salmon experienced a much smaller and gradual rise in plasma total ammonia. Salmon at both temperatures experienced extracellular and intracellular alkalosis within 1 hour that recovered within 24 hours, but the alkalosis was smaller in magnitude in fish at warmer temperature. Impacts on plasma ion concentrations were relatively mild and plasma glucose increased by 2- to 4-fold at both temperatures. Notably, the increase in plasma total ammonia in fish at the warmer temperature was far faster and much greater than those reported in previous studies exposing fish despite higher water pH (9.4-10.5) induced without using ash. This suggests that ash has physiological impacts that cannot be explained by high water pH alone which may relate to the complex mixture of metals and organic compounds also released from ash. This demonstrates post-wildfire ash input can induce lethal yet previously unexplored physiological disturbances in fish and highlights the complex interaction with warmer temperatures typical of wildfire-scarred landscapes.

physiology↗

Rapid blood acid-base regulation by European sea bass (Dicentrarchus labrax) in response to sudden exposure to high environmental CO2

Fish in coastal ecosystems can be exposed to acute variations in CO2 that can approach 1 kPa CO2 (10,000 atm). Coping with this environmental challenge will depend on the ability to rapidly compensate the internal acid-base disturbance caused by sudden exposure to high environmental CO2 (blood and tissue acidosis); however, studies about the speed of acid-base regulatory responses in marine fish are scarce. We observed that upon exposure to ~1 kPa CO2, European sea bass (Dicentrarchus labrax) completely regulate erythrocyte intracellular pH within ~40 minutes, thus restoring haemoglobin-O2 affinity to pre-exposure levels. Moreover, blood pH returned to normal levels within ~2 hours, which is one of the fastest acid-base recoveries documented in any fish. This was achieved via a large upregulation of net acid excretion and accumulation of HCO3- in blood, which increased from ~4 to ~22 mM. While the abundance and intracellular localisation of gill Na+/K+-ATPase (NKA) and Na+/H+ exchanger 3 (NHE3) remained unchanged, the apical surface area of acid-excreting gill ionocytes doubled. This constitutes a novel mechanism for rapidly increasing acid excretion during sudden blood acidosis. Rapid acid-base regulation was completely prevented when the same high CO2 exposure occurred in seawater with experimentally reduced HCO3- and pH, likely because reduced environmental pH inhibited gill H+ excretion via NHE3. The rapid and robust acid-base regulatory responses identified will enable European sea bass to maintain physiological performance during large and sudden CO2 fluctuations that naturally occur in coastal environments. Summary statementEuropean sea bass exposed to 1 kPa (10,000 atm) CO2 regulate blood and red cell pH within 2 hours and 40 minutes, respectively, protecting O2 transport capacity, via enhanced gill acid excretion.

physiology↗

Temperature and O2, but not CO2, interact to affect aerobic performance of European sea bass (Dicentrarchus labrax)

Climate change causes warming, decreased O2, and increased CO2 in marine systems and responses of organisms will depend on interactive effects between these factors. We provide the first experimental assessment of the interactive effects of warming (14 to 22{degrees}C), reduced O2 ([~]3 - 21 kPa O2), and increased CO2 ([~]400 or [~]1000 {micro}atm ambient CO2) on four indicators of aerobic performance (standard metabolic rate, SMR, maximum metabolic rate, MMR, aerobic scope, and hypoxia tolerance, O2crit), blood chemistry, and O2 transport (P50) of a marine fish, the European sea bass (Dicentrarchus labrax). Warming increased SMR and O2crit (i.e. reduced hypoxia tolerance) as well as MMR in normoxia but there was an interactive effect with O2 so that hypoxia caused larger reductions in MMR and aerobic scope at higher temperatures. Increasing CO2 had minimal effects on SMR, MMR and O2crit and did not show interactive effects with temperature or O2 for any measured variables. Aerobic performance was not linked to changes in blood chemistry or P50. Despite lack of effects of CO2 on aerobic performance, increased CO2 induced 30% mortality of fish exercised in low O2 at 22{degrees}C indicating important threshold effects independent of aerobic performance. Overall, our results show temperature and O2, but not CO2, interact to affect aerobic performance of sea bass, disagreeing with predictions of the oxygen- and capacity-limited thermal tolerance hypothesis.

ecology↗