Abstract

A decrease in environmental temperature represents a challenge to the cardiovascular system of ectotherms. To gain insight into the cellular changes that occur during cold exposure and cold acclimation we characterized the cardiac phosphoproteome and proteome of zebrafish following 24 h or one week exposure to 20 oC from 27 oC; or at multiple points during six weeks of acclimation to 20 oC from 27 oC. Our results indicate that cold exposure causes an increase in mitogen-activated protein kinase signaling, the activation of stretch sensitive pathways, cellular remodeling via ubiquitin-dependent pathways, and changes to the phosphorylation state of proteins that regulate myofilament structure and function including desmin and troponin T. Cold acclimation (2-6 weeks) led to a decrease in multiple components of the electron transport chain through time, but an increase in proteins for lipid transport, lipid metabolism, the incorporation of polyunsaturated fatty acids into membranes and protein turnover. For example, there was an increase in the levels of apolipoprotein C, prostaglandin reductase-3, and surfeit locus protein 4, involved in lipid transport, lipid metabolism, and lipid membrane remodeling. Gill opercular movements suggests that oxygen utilization during cold acclimation is reduced. Neither the amount of food consumed relative to body mass nor body condition were affected by acclimation. These results suggest that while oxygen uptake was reduced, energy homeostasis was maintained. This study highlights that the response of zebrafish to a decrease in temperature is dynamic through time and that investment in the proteomic response increases with the duration of exposure.

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