Antarctic notothenioid fishes are noteworthy for their history of isolation and indications they lack the heat shock response. The mechanistic basis for stenothermy has not been fully elucidated, and some aspects of stenothermy could arise post-transcriptionally. Antarctic emerald rockcod (Trematomus bernacchii) were sampled after exposure to chronic and/or acute high temperatures, followed by assessment of proteomic responses in brain, gill, and kidney using tissue-specific DIA assay libraries. Few cellular stress response proteins were induced, and overall responses were modest in terms of numbers of differentially expressed proteins and their fold changes. Inconsistencies in protein induction across treatments and tissues are suggestive of dysregulation, rather than an adaptive response. Changes in regulation of translation in Antarctic notothenioids could explain these patterns. Some components of the “integrative stress response” that regulates translation are highly conserved (e.g., Ser-52 of eIF2α), but the eIF2α kinases GCN2 and PERK may have evolved along different trajectories in Antarctic fishes. Together, these observations suggest a novel hypothesis for stenothermy and the absence of a coordinated cellular stress response in Antarctic fishes.

The experimental design involved sampling Trematomus bernacchii tissues from 8 total treatments (n = 5-6 per treatment): three after acclimation (“chronic”, C), three after an acute thermal ramp from the acclimation temperature (“heat”, H), and two 24 h after an acute heat stress during recovery at the respective acclimation temperature (“recovery”, R). Animals were first acclimated to one of three constant-temperature conditions (-0.4±0.2°C, 2.3±0.2°C, 5.0±0.7°C) for 14 days; for convenience these are referred to as C-1, C+2, and C+5. The highest of these temperatures is close to the acute lethal temperature of wild-caught T. bernacchii, but there was no mortality in our study. This species shows evidence of acclimation of its thermal limits after roughly 1-4 days. A second set of animals experienced each of the three acclimation treatments and was then exposed to an acute temperature ramp (slope = 5°C per hour). Tissues from these three treatments (H-1,H+2, H+5) were sampled as above when each individual fish exhibited cardiac arrhythmia, between ~11.7 and 12.3°C. Finally, for the two lowest temperature acclimation groups we collected a third “recovery” set of tissue samples 24 h after the animals were returned to their respective acclimation temperature following the acute temperature ramp (R-1, R+2).

Three tissues (gill, head kidney, and brain [cerebellum]) were sampled from animals in each of these 8 treatment conditions after the fish were euthanized. Tissues were analyzed separately using tissue-specific DIA assay libraries.