Effect of elevated embryonic incubation temperature on the temperature preference of juvenile lake (Coregonus clupeaformis) and round whitefish (Prosopium cylindraceum).

Anthropogenic impacts can lead to increased temperatures in freshwater environments through thermal effluent and climate change. Thermal preference of aquatic organisms can be modulated by abiotic and biotic factors including environmental temperature. Whether increased temperature during embryogenesis can lead to long-term alterations in thermal preference has not been explicitly tested in native freshwater species. Lake (Coregonus clupeaformis) and round (Prosopium cylindraceum) whitefish were incubated at natural and elevated temperatures until hatching, following which, all groups were moved to common garden conditions (15°C) during the post-hatching stage. Temperature preference was determined at 8 months (Lake whitefish only) and 12 months of age (both species) using a shuttle box system. Round whitefish preferred a cooler temperature when incubated at 2 and 6°C compared with 0.5°C. Lake whitefish had similar temperature preferences regardless of age, weight and incubation temperature. These results reveal that temperature preference in freshwater fish can be programmed during early development, and that round whitefish may be more sensitive to incubation temperature. This study highlights the effects that small increases in temperature caused by anthropogenic impacts may have on cold-adapted freshwater fish.

Hypoxia and High Temperature as Interacting Stressors: Will Plasticity Promote Resilience of Fishes in a Changing World?

AbstractDetermining the resilience of a species or population to climate change stressors is an important but difficult task because resilience can be affected both by genetically based variation and by various types of phenotypic plasticity. In addition, most of what is known about organismal responses is for single stressors in isolation, but environmental change involves multiple environmental factors acting in combination. Here, our goal is to summarize what is known about phenotypic plasticity in fishes in response to high temperature and low oxygen (hypoxia) in combination across multiple timescales, to ask how much resilience plasticity may provide in the face of climate change. There are relatively few studies investigating plasticity in response to these environmental stressors in combination; but the available data suggest that although fish have some capacity to adjust their phenotype and compensate for the negative effects of acute exposure to high temperature and hypoxia through acclimation or developmental plasticity, compensation is generally only partial. There is very little known about intergenerational and transgenerational effects, although studies on each stressor in isolation suggest that both positive and negative impacts may occur. Overall, the capacity for phenotypic plasticity in response to these two stressors is highly variable among species and extremely dependent on the specific context of the experiment, including the extent and timing of stressor exposure. This variability in the nature and extent of plasticity suggests that existing phenotypic plasticity is unlikely to adequately buffer fishes against the combined stressors of high temperature and hypoxia as our climate warms.

Evaluating tank acclimation and trial length for dynamic shuttle box temperature preference assays in aquatic animals.

Characterizing the thermal preference of fish is important in conservation, environmental and evolutionary physiology and can be determined using a shuttle box system. Initial tank acclimation and trial lengths are important considerations in experimental design, yet systematic studies of these factors are missing. Three different behavioral assay experimental designs were tested to determine the effect of tank acclimation and trial length (hours of tank acclimation:behavioral trial: 12:12, 0:12, 2:2) on the temperature preference of juvenile lake whitefish (Coregonus clupeaformis), using a shuttle box. Average temperature preferences for the 12 h:12 h, 0 h:12 h, 2 h:2 h experimental designs were 16.10±1.07°C, 16.02±1.56°C and 16.12±1.59°C respectively, with no significant differences between experimental designs (P=0.9337). Ultimately, length of acclimation time and trial length had no significant effect on thermal preference.

Osteopontin deficiency increases bone fragility but preserves bone mass.

The ability of bone to resist catastrophic failure is critically dependent upon the material properties of bone matrix, a composite of hydroxyapatite, collagen type I, and noncollagenous proteins. These properties include elastic modulus, hardness, and fracture toughness. Like other aspects of bone quality, matrix material properties are biologically-defined and can be disrupted in skeletal disease. While mineral and collagen have been investigated in greater detail, the contribution of noncollagenous proteins such as osteopontin to bone matrix material properties remains unclear. Several roles have been ascribed to osteopontin in bone, many of which have the potential to impact material properties. To elucidate the role of osteopontin in bone quality, we evaluated the structure, composition, and material properties of bone from osteopontin-deficient mice and wild-type littermates at several length scales. Most importantly, the results show that osteopontin deficiency causes a 30% decrease in fracture toughness, suggesting an important role for OPN in preventing crack propagation. This significant decline in fracture toughness is independent of changes in whole bone mass, structure, or matrix porosity. Using nanoindentation and quantitative backscattered electron imaging to evaluate osteopontin-deficient bone matrix at the micrometer level, we observed a significant reduction in elastic modulus and increased variability in calcium concentration. Matrix heterogeneity was also apparent at the ultrastructural level. In conclusion, we find that osteopontin is essential for the fracture toughness of bone, and reduced toughness in osteopontin-deficient bone may be related to the increased matrix heterogeneity observed at the micro-scale. By exploring the effects of osteopontin deficiency on bone matrix material properties, composition and organization, this study suggests that reduced fracture toughness is one mechanism by which loss of noncollagenous proteins contribute to bone fragility.