Temperature during embryonic development has persistent effects on metabolic enzymes in the muscle of zebrafish

• Published in: Journal of experimental biology Vol. 217; no. Pt 8; pp. 1370 - 1380
• Main Authors: Schnurr, Meghan E, Yin, Yi, Scott, Graham R
• Format: Journal Article
• Language: English
• Published: England 15.04.2014
• Subjects: Acclimatization; Animals; Embryo, Nonmammalian - embryology; Embryo, Nonmammalian - enzymology; Embryonic Development; Energy Metabolism; Female; Male; Muscle, Skeletal - enzymology; Temperature; Zebrafish - embryology; Zebrafish - physiology; Phenotypic plasticity; Acclimatization; Developmental plasticity; Thermal performance curve; Muscle phenotype
• ISSN: 0022-0949; 1477-9145
• DOI: 10.1242/jeb.094037

Global warming is intensifying interest in the physiological consequences of temperature change in ectotherms, but we still have a relatively poor understanding of the effects of temperature on early life stages. This study determined how embryonic temperature (TE) affects development and the activity of metabolic enzymes in the swimming muscle of zebrafish. Embryos developed successfully to hatching (survival ≥ 88%) from 22 to 32°C, but suffered sharp increases in mortality outside of this range. Embryos that were incubated until hatching at a control TE (27°C) or near the extremes for successful development (22 or 32°C) were next raised to adulthood under control conditions at 27°C. Growth trajectories after hatching were altered in the 22°C and 32°C TE groups compared with 27°C TE controls, but growth slowed after 3 months of age in all groups. Maximal enzyme activities of cytochrome c oxidase (COX), citrate synthase (CS), hydroxyacyl-coA dehydrogenase (HOAD), pyruvate kinase (PK) and lactate dehydrogenase (LDH) were measured across a range of assay temperatures (22, 27, 32 and 36°C) in adults from each TE group that were acclimated to 27 or 32°C. Substrate affinities (Km) were also determined for COX and LDH. In adult fish acclimated to 27°C, COX and PK activities were higher in 22°C and 32°C TE groups than in 27°C TE controls, and the temperature optimum for COX activity was higher in the 32°C TE group than in the 22°C TE group. Warm acclimation reduced COX, CS and/or PK activities in the 22 and 32°C TE groups, possibly to compensate for thermal effects on molecular activity. This response did not occur in the 27°C TE controls, which instead increased LDH and HOAD activities. Warm acclimation also increased thermal sensitivity (Q10) of HOAD to cool temperatures across all TE groups. We conclude that the temperature experienced during early development can have a persistent impact on energy metabolism pathways and acclimation capacity in later life.