Overcoming the coupled climate and biodiversity crises and their societal impacts.

Earth's biodiversity and human societies face pollution, overconsumption of natural resources, urbanization, demographic shifts, social and economic inequalities, and habitat loss, many of which are exacerbated by climate change. Here, we review links among climate, biodiversity, and society and develop a roadmap toward sustainability. These include limiting warming to 1.5°C and effectively conserving and restoring functional ecosystems on 30 to 50% of land, freshwater, and ocean "scapes." We envision a mosaic of interconnected protected and shared spaces, including intensively used spaces, to strengthen self-sustaining biodiversity, the capacity of people and nature to adapt to and mitigate climate change, and nature's contributions to people. Fostering interlinked human, ecosystem, and planetary health for a livable future urgently requires bold implementation of transformative policy interventions through interconnected institutions, governance, and social systems from local to global levels.

The human imperative of stabilizing global climate change at 1.5°C.

Increased concentrations of atmospheric greenhouse gases have led to a global mean surface temperature 1.0°C higher than during the pre-industrial period. We expand on the recent IPCC Special Report on global warming of 1.5°C and review the additional risks associated with higher levels of warming, each having major implications for multiple geographies, climates, and ecosystems. Limiting warming to 1.5°C rather than 2.0°C would be required to maintain substantial proportions of ecosystems and would have clear benefits for human health and economies. These conclusions are relevant for people everywhere, particularly in low- and middle-income countries, where the escalation of climate-related risks may prevent the achievement of the United Nations Sustainable Development Goals.

Exposure history determines pteropod vulnerability to ocean acidification along the US West Coast.

The pteropod Limacina helicina frequently experiences seasonal exposure to corrosive conditions (Ωar < 1) along the US West Coast and is recognized as one of the species most susceptible to ocean acidification (OA). Yet, little is known about their capacity to acclimatize to such conditions. We collected pteropods in the California Current Ecosystem (CCE) that differed in the severity of exposure to Ωar conditions in the natural environment. Combining field observations, high-CO2 perturbation experiment results, and retrospective ocean transport simulations, we investigated biological responses based on histories of magnitude and duration of exposure to Ωar < 1. Our results suggest that both exposure magnitude and duration affect pteropod responses in the natural environment. However, observed declines in calcification performance and survival probability under high CO2 experimental conditions do not show acclimatization capacity or physiological tolerance related to history of exposure to corrosive conditions. Pteropods from the coastal CCE appear to be at or near the limit of their physiological capacity, and consequently, are already at extinction risk under projected acceleration of OA over the next 30 years. Our results demonstrate that Ωar exposure history largely determines pteropod response to experimental conditions and is essential to the interpretation of biological observations and experimental results.

Intra-population variability of ocean acidification impacts on the physiology of Baltic blue mussels (Mytilus edulis): integrating tissue and organism response.

Increased maintenance costs at cellular, and consequently organism level, are thought to be involved in shaping the sensitivity of marine calcifiers to ocean acidification (OA). Yet, knowledge of the capacity of marine calcifiers to undergo metabolic adaptation is sparse. In Kiel Fjord, blue mussels thrive despite periodically high seawater PCO2, making this population interesting for studying metabolic adaptation under OA. Consequently, we conducted a multi-generation experiment and compared physiological responses of F1 mussels from 'tolerant' and 'sensitive' families exposed to OA for 1 year. Family classifications were based on larval survival; tolerant families settled at all PCO2 levels (700, 1120, 2400 µatm) while sensitive families did not settle at the highest PCO2 (≥99.8% mortality). We found similar filtration rates between family types at the control and intermediate PCO2 level. However, at 2400 µatm, filtration and metabolic scope of gill tissue decreased in tolerant families, indicating functional limitations at the tissue level. Routine metabolic rates (RMR) and summed tissue respiration (gill and outer mantle tissue) of tolerant families were increased at intermediate PCO2, indicating elevated cellular homeostatic costs in various tissues. By contrast, OA did not affect tissue and routine metabolism of sensitive families. However, tolerant mussels were characterised by lower RMR at control PCO2 than sensitive families, which had variable RMR. This might provide the energetic scope to cover increased energetic demands under OA, highlighting the importance of analysing intra-population variability. The mechanisms shaping such difference in RMR and scope, and thus species' adaptation potential, remain to be identified.

Ocean warming and acidification modulate energy budget and gill ion regulatory mechanisms in Atlantic cod (Gadus morhua).

Ocean warming and acidification are threatening marine ecosystems. In marine animals, acidification is thought to enhance ion regulatory costs and thereby baseline energy demand, while elevated temperature also increases baseline metabolic rate. Here we investigated standard metabolic rates (SMR) and plasma parameters of Atlantic cod (Gadus morhua) after 3-4 weeks of exposure to ambient and future PCO2 levels (550, 1200 and 2200 µatm) and at two temperatures (10, 18 °C). In vivo branchial ion regulatory costs were studied in isolated, perfused gill preparations. Animals reared at 18 °C responded to increasing CO2 by elevating SMR, in contrast to specimens at 10 °C. Isolated gills at 10 °C and elevated PCO2 (≥1200 µatm) displayed increased soft tissue mass, in parallel to increased gill oxygen demand, indicating an increased fraction of gill in whole animal energy budget. Altered gill size was not found at 18 °C, where a shift in the use of ion regulation mechanisms occurred towards enhanced Na(+)/H(+)-exchange and HCO3 (-) transport at high PCO2 (2200 µatm), paralleled by higher Na(+)/K(+)-ATPase activities. This shift did not affect total gill energy consumption leaving whole animal energy budget unaffected. Higher Na(+)/K(+)-ATPase activities in the warmth might have compensated for enhanced branchial permeability and led to reduced plasma Na(+) and/or Cl(-) concentrations and slightly lowered osmolalities seen at 18 °C and 550 or 2200 µatm PCO2 in vivo. Overall, the gill as a key ion regulation organ seems to be highly effective in supporting the resilience of cod to effects of ocean warming and acidification.

OCEANOGRAPHY. Contrasting futures for ocean and society from different anthropogenic CO2 emissions scenarios.

The ocean moderates anthropogenic climate change at the cost of profound alterations of its physics, chemistry, ecology, and services. Here, we evaluate and compare the risks of impacts on marine and coastal ecosystems­and the goods and services they provide­for growing cumulative carbon emissions under two contrasting emissions scenarios. The current emissions trajectory would rapidly and significantly alter many ecosystems and the associated services on which humans heavily depend. A reduced emissions scenario­consistent with the Copenhagen Accord's goal of a global temperature increase of less than 2°C­is much more favorable to the ocean but still substantially alters important marine ecosystems and associated goods and services. The management options to address ocean impacts narrow as the ocean warms and acidifies. Consequently, any new climate regime that fails to minimize ocean impacts would be incomplete and inadequate.

Differential impacts of elevated CO2 and acidosis on the energy budget of gill and liver cells from Atlantic cod, Gadus morhua.

Ocean acidification impacts fish and other marine species through increased seawater PCO2 levels (hypercapnia). Knowledge of the physiological mechanisms mediating effects in various tissues of fish is incomplete. Here we tested the effects of extracellular hypercapnia and acidosis on energy metabolism of gill and liver cells of Atlantic cod. Exposure media mimicked blood conditions in vivo, either during normo- or hypercapnia and at control or acidic extracellular pH (pHe). We determined metabolic rate and energy expenditure for protein biosynthesis, Na(+)/K(+)-ATPase and H(+)-ATPase and considered nutrition status by measurements of metabolic rate and protein biosynthesis in media with and without free amino acids (FAA). Addition of FAA stimulated hepatic but not branchial oxygen consumption. Normo- and hypercapnic acidosis as well as hypercapnia at control pHe depressed metabolic stimulation of hepatocytes. In gill cells, acidosis depressed respiration independent of PCO2 and FAA levels. For both cell types, depressed respiration was not correlated with the same reduction in energy allocated to protein biosynthesis or Na(+)/K(+)-ATPase. Hepatic energy expenditure for protein synthesis and Na(+)/K(+)-ATPase was even elevated at acidic compared to control pHe suggesting increased costs for ion regulation and cellular reorganization. Hypercapnia at control pHe strongly reduced oxygen demand of branchial Na(+)/K(+)-ATPase with a similar trend for H(+)-ATPase. We conclude that extracellular acidosis triggers metabolic depression in gill and metabolically stimulated liver cells. Additionally, hypercapnia itself seems to limit capacities for metabolic usage of amino acids in liver cells while it decreases the use and costs of ion regulatory ATPases in gill cells.

Stress response or beneficial temperature acclimation: transcriptomic signatures in Antarctic fish (Pachycara brachycephalum).

Research on the thermal biology of Antarctic marine organisms has increased awareness of their vulnerability to climate change, as a flipside of their adaptation to life in the permanent cold and their limited capacity to acclimate to variable temperatures. Here, we employed a species-specific microarray of the Antarctic eelpout, Pachycara brachycephalum, to identify long-term shifts in gene expression after 2 months of acclimation to six temperatures between -1 and 9 °C. Changes in cellular processes comprised signalling, post-translational modification, cytoskeleton remodelling, metabolic shifts and alterations in the transcription as well as translation machinery. The magnitude of transcriptomic responses paralleled the change in whole animal performance. Optimal growth at 3 °C occurred at a minimum in gene expression changes indicative of a balanced steady state. The up-regulation of ribosomal transcripts at 5 °C and above was accompanied by the transcriptomic activation of differential protein degradation pathways, from proteasome-based degradation in the cold towards lysosomal protein degradation in the warmth. From 7 °C upwards, increasing transcript levels representing heat-shock proteins and an acute inflammatory response indicate cellular stress. Such patterns may contribute to a warm-induced energy deficit and a strong weight loss at temperatures above 6 °C. Together, cold or warm acclimation led to specific cellular rearrangements and the progressive development of functional imbalances beyond the optimum temperature. The observed temperature-specific expression profiles reveal the molecular basis of thermal plasticity and refine present understanding of the shape and positioning of the thermal performance curve of ectotherms on the temperature scale.

Climate change effects on fishes and fisheries: towards a cause-and-effect understanding.

Ongoing climate change is predicted to affect individual organisms during all life stages, thereby affecting populations of a species, communities and the functioning of ecosystems. These effects of climate change can be direct, through changing water temperatures and associated phenologies, the lengths and frequency of hypoxia events, through ongoing ocean acidification trends or through shifts in hydrodynamics and in sea level. In some cases, climate interactions with a species will also, or mostly, be indirect and mediated through direct effects on key prey species which change the composition and dynamic coupling of food webs. Thus, the implications of climate change for marine fish populations can be seen to result from phenomena at four interlinked levels of biological organization: (1) organismal-level physiological changes will occur in response to changing environmental variables such as temperature, dissolved oxygen and ocean carbon dioxide levels. An integrated view of relevant effects, adaptation processes and tolerance limits is provided by the concept of oxygen and capacity-limited thermal tolerance (OCLT). (2) Individual-level behavioural changes may occur such as the avoidance of unfavourable conditions and, if possible, movement into suitable areas. (3) Population-level changes may be observed via changes in the balance between rates of mortality, growth and reproduction. This includes changes in the retention or dispersion of early life stages by ocean currents, which lead to the establishment of new populations in new areas or abandonment of traditional habitats. (4) Ecosystem-level changes in productivity and food web interactions will result from differing physiological responses by organisms at different levels of the food web. The shifts in biogeography and warming-induced biodiversity will affect species productivity and may, thus, explain changes in fisheries economies. This paper tries to establish links between various levels of biological organization by means of addressing the effective physiological principles at the cellular, tissue and whole organism levels.

Niche dimensions in fishes: an integrative view.

Current shifts in ecosystem composition and function emphasize the need for an understanding of the links between environmental factors and organism fitness and tolerance. The examples discussed here illustrate how recent progress in the field of comparative physiology may provide a better mechanistic understanding of the ecological concepts of the fundamental and realized niches and thus provide insights into the impacts of anthropogenic disturbance. Here we argue that, as a link between physiological and ecological indicators of organismal performance, the mechanisms shaping aerobic scope and passive tolerance set the dimensions of an animal's niche, here defined as its capacity to survive, grow, behave, and interact with other species. We demonstrate how comparative studies of cod or killifish populations in a latitudinal cline have unraveled mitochondrial mechanisms involved in establishing a species' niche, performance, and energy budget. Riverine fish exemplify how the performance windows of various developmental stages follow the dynamic regimes of both seasonal temperatures and river hydrodynamics, as synergistic challenges. Finally, studies of species in extreme environments, such as the tilapia of Lake Magadi, illustrate how on evolutionary timescales functional and morphological shifts can occur, associated with new specializations. We conclude that research on the processes and time course of adaptations suitable to overcome current niche limits is urgently needed to assess the resilience of species and ecosystems to human impact, including the challenges of global climate change.

Oxygen- and capacity-limitation of thermal tolerance: a matrix for integrating climate-related stressor effects in marine ecosystems.

The concept of oxygen- and capacity-dependent thermal tolerance in aquatic ectotherms has successfully explained climate-induced effects of rising temperatures on species abundance in the field. Oxygen supply to tissues and the resulting aerobic performance characters thus form a primary link between organismal fitness and its role and functioning at the ecosystem level. The thermal window of performance in water breathers matches their window of aerobic scope. Loss of performance reflects the earliest level of thermal stress, caused by hypoxaemia and the progressive mismatch of oxygen supply and demand at the borders of the thermal envelope. Oxygen deficiency elicits the transition to passive tolerance and associated systemic and cellular stress signals like hormonal responses or oxidative stress as well as the use of protection mechanisms like heat shock proteins at thermal extremes. Thermal acclimatization between seasons or adaptation to a climate regime involves shifting thermal windows and adjusting window widths. The need to specialize on a limited temperature range results from temperature-dependent trade-offs at several hierarchical levels, from molecular structure to whole-organism functioning, and may also support maximized energy efficiency. Various environmental factors like CO(2) (ocean acidification) and hypoxia interact with these principal relationships. Existing knowledge suggests that these factors elicit metabolic depression supporting passive tolerance to thermal extremes. However, they also exacerbate hypoxaemia, causing a narrowing of thermal performance windows and prematurely leading the organism to the limits of its thermal acclimation capacity. The conceptual analysis suggests that the relationships between energy turnover, the capacities of activity and other functions and the width of thermal windows may lead to an integrative understanding of specialization on climate and, as a thermal matrix, of sensitivity to climate change and the factors involved. Such functional relationships might also relate to climate-induced changes in species interactions and, thus, community responses at the ecosystem level.

Acid-base regulatory ability of the cephalopod (Sepia officinalis) in response to environmental hypercapnia.

Acidification of ocean surface waters by anthropogenic carbon dioxide (CO(2)) emissions is a currently developing scenario that warrants a broadening of research foci in the study of acid-base physiology. Recent studies working with environmentally relevant CO(2) levels, indicate that some echinoderms and molluscs reduce metabolic rates, soft tissue growth and calcification during hypercapnic exposure. In contrast to all prior invertebrate species studied so far, growth trials with the cuttlefish Sepia officinalis found no indication of reduced growth or calcification performance during long-term exposure to 0.6 kPa CO(2). It is hypothesized that the differing sensitivities to elevated seawater pCO(2) could be explained by taxa specific differences in acid-base regulatory capacity. In this study, we examined the acid-base regulatory ability of S. officinalis in vivo, using a specially modified cannulation technique as well as (31)P NMR spectroscopy. During acute exposure to 0.6 kPa CO(2), S. officinalis rapidly increased its blood [HCO(3)(-)] to 10.4 mM through active ion-transport processes, and partially compensated the hypercapnia induced respiratory acidosis. A minor decrease in intracellular pH (pH(i)) and stable intracellular phosphagen levels indicated efficient pH(i) regulation. We conclude that S. officinalis is not only an efficient acid-base regulator, but is also able to do so without disturbing metabolic equilibria in characteristic tissues or compromising aerobic capacities. The cuttlefish did not exhibit acute intolerance to hypercapnia that has been hypothesized for more active cephalopod species (squid). Even though blood pH (pHe) remained 0.18 pH units below control values, arterial O(2) saturation was not compromised in S. officinalis because of the comparatively lower pH sensitivity of oxygen binding to its blood pigment. This raises questions concerning the potentially broad range of sensitivity to changes in acid-base status amongst invertebrates, as well as to the underlying mechanistic origins. Further studies are needed to better characterize the connection between acid-base status and animal fitness in various marine species.

Temperature-dependent lipid levels and components in polar and temperate eelpout (Zoarcidae).

Total lipid content, lipid classes and fatty acid composition were analysed in tissues from two eelpout species fed on the same diet, the Antarctic Pachycara brachycephalum and the temperate Zoarces viviparus, with the aim of determining the role of lipids in fishes from different thermal habitats. The lipid content increased with decreasing temperature in the liver of both species, suggesting enhanced lipid storage under cold conditions. In P. brachycephalum, lipid composition in the liver and muscle was strongly dominated by triacylglycerols between 0 and 6 degrees C. In contrast, in the temperate species, lipid class composition changed with changes in the temperature. When acclimatized to 4 and 6 degrees C Z. viviparus not only displayed a shift to lipid anabolism and pronounced lipid storage, as indicated by high triacylglycerol levels, but also a shift to patterns of cold adaptation, as reflected by an increased content of polyunsaturated fatty acids in the lipid extract. Unsaturated fatty acids were also abundant in the Antarctic eelpout, but when compared to Z. viviparus at the same temperatures, the latter had significantly higher ratios of polyunsaturated to saturated fatty acid levels, whereas the Antarctic eelpout showed significantly higher ratios of monounsaturated to saturated fatty acid levels. High delta-15N values of the Antarctic eelpout reflect the high trophic level of this scavenger in the Weddell Sea food web. Stable carbon values suggest that lipid-enriched prey forms a major part of its diet. The strategy to accumulate storage lipids in the cold is interpreted to be adaptive behaviour at colder temperatures and during periods of irregular, pulsed food supply.

Effects of hypoxia on the energy status and nitrogen metabolism of African lungfish during aestivation in a mucus cocoon.

We examined the energy status, nitrogen metabolism and hepatic glutamate dehydrogenase activity in the African lungfish Protopterus annectens during aestivation in normoxia (air) or hypoxia (2% O(2) in N(2)), with tissues sampled on day 3 (aerial exposure with preparation for aestivation), day 6 (entering into aestivation) or day 12 (undergoing aestivation). There was no accumulation of ammonia in tissues of fish exposed to normoxia or hypoxia throughout the 12-day period. Ammonia toxicity was avoided by increased urea synthesis and/or decreased endogenous N production (as ammonia), but the dependency on these two mechanisms differed between the normoxic and the hypoxic fish. The rate of urea synthesis increased 2.4-fold, with only a 12% decrease in the rate of N production in the normoxic fish. By contrast, the rate of N production in the hypoxic fish decreased by 58%, with no increase in the rate of urea synthesis. Using in vivo (31)P NMR spectroscopy, it was demonstrated that hypoxia led to significantly lower ATP concentration on day 12 and significantly lower creatine phosphate concentration on days 1, 6, 9 and 12 in the anterior region of the fish as compared with normoxia. Additionally, the hypoxic fish had lower creatine phosphate concentration in the middle region than the normoxic fish on day 9. Hence, lowering the dependency on increased urea synthesis to detoxify ammonia, which is energy intensive by reducing N production, would conserve cellular energy during aestivation in hypoxia. Indeed, there were significant increases in glutamate concentrations in tissues of fish aestivating in hypoxia, which indicates decreases in its degradation and/or transamination. Furthermore, there were significant increases in the hepatic glutamate dehydrogenase (GDH) amination activity, the amination/deamination ratio and the dependency of the amination activity on ADP activation in fish on days 6 and 12 in hypoxia, but similar changes occurred only in the normoxic fish on day 12. Therefore, our results indicate for the first time that P. annectens exhibited different adaptive responses during aestivation in normoxia and in hypoxia. They also indicate that reduction in nitrogen metabolism, and probably metabolic rate, did not occur simply in association with aestivation (in normoxia) but responded more effectively to a combined effect of aestivation and hypoxia.

Cold induced changes of adenosine levels in common eelpout (Zoarces viviparus): a role in modulating cytochrome c oxidase expression.

Exposure of ectothermic organisms to variations in temperatures causes a transient mismatch between energy supply and demand, which needs to be compensated for during acclimation. Adenosine accumulation from ATP breakdown indicates such an imbalance and its reversal reflects a restoration of energy status. We monitored adenosine levels in blood serum and liver of common eelpout (Zoarces viviparus) during cold exposure in vivo. Furthermore, we tested its effect on the pattern of thermal acclimation in hepatocytes isolated from cold- (4 degrees C) versus warm- (11 degrees C) exposed fish. Adenosine levels increased during cold exposure in vivo and reached a transient maximum after 24 h in serum, but remained permanently elevated in liver. Whole animal cold acclimation induced a rise of liver citrate synthase activity by 44+/-15%, but left cytochrome c oxidase activity (COX) and RNA expression of the respective genes unchanged. Cold incubation of hepatocytes from warm-acclimated fish failed to cause an increase of mitochondrial enzyme activities despite increased COX4 mRNA levels. Conversely, warm acclimation of hepatocytes from cold-acclimated fish reduced both enzyme activities and COX2 and COX4 mRNA levels by 26-37%. Adenosine treatment of both warm- and cold-acclimated hepatocytes suppressed COX activities but activated COX mRNA expression. These effects were not receptor mediated. The present findings indicate that adenosine has the potential to regulate mitochondrial functioning in vivo, albeit the pathways resulting in the contrasting effects on expression and activity need to be identified.

Effects of seasonal and latitudinal cold on oxidative stress parameters and activation of hypoxia inducible factor (HIF-1) in zoarcid fish.

Acute, short term cooling of North Sea eelpout Zoarces viviparus is associated with a reduction of tissue redox state and activation of hypoxia inducible factor (HIF-1) in the liver. The present study explores the response of HIF-1 to seasonal cold in Zoarces viviparus, and to latitudinal cold by comparing the eurythermal North Sea fish to stenothermal Antarctic eelpout (Pachycara brachycephalum). Hypoxic signalling (HIF-1 DNA binding activity) was studied in liver of summer and winter North Sea eelpout as well as of Antarctic eelpout at habitat temperature of 0 degrees C and after long-term warming to 5 degrees C. Biochemical parameters like tissue iron content, glutathione redox ratio, and oxidative stress indicators were analyzed to see whether the cellular redox state or reactive oxygen species formation and HIF activation in the fish correlate. HIF-1 DNA binding activity was significantly higher at cold temperature, both in the interspecific comparison, polar vs. temperate species, and when comparing winter and summer North Sea eelpout. Compared at the low acclimation temperatures (0 degrees C for the polar and 6 degrees C for the temperate eelpout) the polar fish showed lower levels of lipid peroxidation although the liver microsomal fraction turned out to be more susceptible to lipid radical formation. The level of radical scavenger, glutathione, was twofold higher in polar than in North Sea eelpout and also oxidised to over 50%. Under both conditions of cold exposure, latitudinal cold in the Antarctic and seasonal cold in the North Sea eelpout, the glutathione redox ratio was more oxidised when compared to the warmer condition. However, oxidative damage parameters (protein carbonyls and thiobarbituric acid reactive substances (TBARS) were elevated only during seasonal cold exposure in Z. viviparus. Obviously, Antarctic eelpout are keeping oxidative defence mechanisms high enough to avoid accumulation of oxidative damage products at low habitat temperature. The paper discusses how HIF could be instrumental in cold adaptation in fish.

Effects of environmental hypercapnia on animal physiology: a 13C NMR study of protein synthesis rates in the marine invertebrate Sipunculus nudus.

Global climate change is associated with a progressive rise in ocean CO(2) concentrations (hypercapnia) and, consequently, a drop in seawater pH. However, a comprehensive picture of the physiological mechanisms affected by chronic CO(2) stress in marine biota is still lacking. Here we present an analysis of protein biosynthesis rates in isolated muscle of the marine invertebrate Sipunculus nudus, a sediment dwelling worm living at various water depths. We followed the incorporation of (13)C-labelled phenylalanine into muscular protein via high-resolution NMR spectroscopy. Protein synthesis decreased by about 60% at a medium pH of 6.70 and a consequently lowered intracellular pH (pHi). The decrease in protein synthesis rates is much stronger than the concomitant suppression of protein degradation (60% versus 10-15%) possibly posing a threat to the cellular homeostasis of structural as well as functional proteins. Considering the progressive rise in ocean CO(2) concentrations, permanent disturbances of cellular protein turnover might seriously affect growth and reproductive performance in many marine organisms with as yet unexplored impacts on species density and composition in marine ecosystems.

Mitochondrial mechanisms of cold adaptation in cod (Gadus morhua L.) populations from different climatic zones.

Adjustments in mitochondrial properties and capacities are crucial in acclimatization to seasonal cold as well as in evolutionary cold adaptation of marine ectotherms. To examine whether gene expression mechanisms contribute to different settings of aerobic capacities in populations of cod (Gadus morhua) along a latitudinal cline, maximum activities of key enzymes of mitochondrial metabolism and their respective mRNA levels were compared in white muscle and liver of cold (4 degrees C) and warm (10 degrees C) acclimated individuals from cod populations of the North Sea and the Barents Sea, respectively. In white muscle, cold acclimation caused a parallel increase in citrate synthase (CS) and in cytochrome c oxidase (COX) activities, but with a much larger effect in the cold eurythermal Arctic population. In liver, cold acclimation was accompanied by increments in CS activities, but differences between populations were minor. Overall COX activities in liver were not affected by cold acclimation, but were higher in the cold adapted population. In both populations increments in muscle CS capacities were tightly correlated with elevated mRNA levels, suggesting transcriptional control of citrate synthase levels in muscle. In liver, CS mRNA levels differed between populations but were not affected by cold acclimation, so that post-transcriptional control may contribute to elevated functional levels in this tissue. Mitochondrial-encoded COX2 mRNA levels were not limiting for functional activities in both tissues, in favour of post-transcriptional control or limitations by other transcripts of the COX complex. Altogether, the differentiation in gene expression between both populations was more strongly expressed at 4 degrees C. The comparison of functional levels and transcript levels may reflect genetic differentiation at functional sites, in line with genetic differences between the two populations previously established by non-coding genetic markers.

The strengths of in vivo magnetic resonance imaging (MRI) to study environmental adaptational physiology in fish.

Adaptational physiology studies how animals cope with their environment, even if this environment is subject to permanent fluctuations such as tidal or seasonal variations. Aquatic organisms are generally more prone to be exposed to osmotic, hypoxic and temperature challenges than terrestrial animals. Some of these challenges are more restraining in an aquatic environment. To date, very few studies have used in vivo magnetic resonance imaging (MRI) to uncover the physiological mechanisms that respond to or compensate for these challenges. This paper provides an overview of what has been accomplished thus far by using MRI to study the environmental physiology of fish. It introduces the reader to the use of small teleost fish such as carp (12 cm, 60 g) and eelpout (25 cm, 50 g) as models for such research and to provide new perceptions into the applicability of MRI tools based on new insights into the nature of MRI contrast. Representative MRI studies have made contributions to the identification of the lack of cell volume repair in stenohaline fish during osmotic stress. They have studied the underlying physiological mechanisms of brain anoxia tolerance in fish and have qualified the role of the cardio-circulatory system in setting thermal tolerance windows of fish.

High sensitivity to chronically elevated CO2 levels in a eurybathic marine sipunculid.

CO2 levels are expected to rise (a) in surface waters of the oceans as atmospheric accumulation continues or (b) in the deep sea, once industrial CO2 dumping is implemented. These scenarios suggest that CO2 will become a general stress factor in aquatic environments. The mechanisms of sensitivity to CO2 as well as adaptation capacity of marine animals are insufficiently understood. Here, we present data obtained in Sipunculus nudus, a sediment-dwelling marine worm that is able to undergo drastic metabolic depression to survive regular exposure to elevated CO2 levels within its natural habitat. We investigated animal survival and the proximate biochemical body composition during long-term CO2 exposure. Results indicate an unexpected and pronounced sensitivity characterized by the delayed onset of enhanced mortality at CO2 levels within the natural range of concentrations. Therefore, the present study contrasts the previously assumed high-CO2 tolerance of animals adapted to temporary hypercapnia. As a consequence, we expect future loss of species and, thereby, detrimental effects on marine benthic ecosystems with as yet poorly defined critical thresholds of long-term tolerance to CO2.