Physiological plasticity v. inter-population variability: Understanding drivers of hypoxia tolerance in a tropical estuarine fish

Physiological plasticity and inter-population variability (e.g. local adaptation) are two key drivers in determining the capacity for species to cope with environmental change, yet the relative contribution of each parameter has received little attention. Here, we investigate the acclimation potential of two geographically distinct populations of the barramundi (Lates calcarifer) to diel hypoxia. Fish were exposed to a daily hypoxia challenge of 6h below 62% saturation, down to a minimum of 10±5% saturation, followed by a return to normoxia. Respiratory and haematological variables were assessed after 8 and 16 days of daily hypoxia exposure. Hypoxia tolerance (measured as the critical oxygen tension; [O2]crit) was not different between populations and not different from control fish after 8 days ([O2]crit≤20.7±2.8% saturation), but improved similarly in both populations after 16 days ([O2]crit≤16.5±3.1% saturation). This improvement corresponded with increases in haematocrit and haemoglobin, but not an increase in the mean cell haemoglobin concentration. Given the similarity of the response between these two geographically distinct populations, we conclude that hypoxia tolerance for barramundi may be more dependent on physiological plasticity than inherent variability between populations. © CSIRO 2016

Hypoxia tolerance is conserved across genetically distinct sub-populations of an iconic, tropical Australian teleost (Lates calcarifer)

Tropical coastal systems are particularly prone to periods of environmental hypoxia, which can result from organismal respiration as well as thermal stratification, and may be further exacerbated by anthropogenic disturbances. In this study, we used five genetically distinct sub-populations of Australian barramundi (Lates calcarifer) to examine the extent of intraspecific variability in hypoxia tolerance. Fish were maintained at two temperatures (26 or 36°C), representing the seasonal thermal range for this species across its tropical distribution in Australia. All fish maintained a constant oxygen consumption rate (M˙O2) as air saturation of the water decreased from 100% down to a critical oxygen saturation ([O2]crit) of 15.44 ± 3.20 and 21.07 ± 3.92% (means ± SD) at 26 and 36°C, respectively. Mean [O2]crit, used as a performance measure of hypoxia tolerance, did not differ between sub-populations. No differences were found for resting M˙O2 between sub-populations at 26°C, but modest differences were detected between two sub-populations at 36°C (3.36 ± 0.62 and 2.83 ± 0.27 mg O2 kg-1 min-1 for Gladstone and Broome sub-populations, respectively). Resting M˙ O2 was lower for sub-populations at 26°C (1.46 ± 0.26 mg O2 kg-1 min-1) than at 36°C (3.10 ± 0.43 mg O2 kg-1 min-1), with a temperature coefficient (Q10) of 2.12 ± 0.30. We conclude that both hypoxia tolerance and resting M˙O2 are conserved across the distribution of barramundi in Australia, which reflects the capacity of this species to cope in environments with large fluctuations in both temperature and dissolved oxygen

Paternal dietary macronutrient balance and energy intake drive metabolic and behavioral differences among offspring

Paternal diet can influence the phenotype of the next generation, yet, the dietary components inducing specific responses in the offspring are not identified. Here, we use the Nutritional Geometry Framework to determine the effects of pre-conception paternal dietary macronutrient balance on offspring metabolic and behavioral traits in mice. Ten isocaloric diets varying in the relative proportion of protein, fats, and carbohydrates are fed to male mice prior to mating. Dams and offspring are fed standard chow and never exposed to treatment diets. Body fat in female offspring is positively associated with the paternal consumption of fat, while in male offspring, an anxiety-like phenotype is associated to paternal diets low in protein and high in carbohydrates. Our study uncovers that the nature and the magnitude of paternal effects are driven by interactions between macronutrient balance and energy intake and are not solely the result of over- or undernutrition