Gene expression pattern in the liver during recovery from an acute stressor in rainbow trout.

The physiological response to stressors, including hormonal profiles and associated tissue responsiveness, has been extensively studied with salmonid fish, but less is known about the molecular basis of this adaptive response. As liver is the major target organ for metabolic adjustments, we exploited a selective transcriptomics approach to address molecular response in this tissue during acute stress adaptation in rainbow trout. The stressor consisted of a standardized 3 min handling disturbance of trout, and plasma and liver samples were collected either prior to or 1 and 24 h after stressor exposure. We developed a low density custom cDNA array consisting of 147 rainbow trout genes designed specifically to represent stress-responsive and endocrine-related pathways in fish. The acute stress response and recovery was confirmed by the transient elevation in plasma cortisol concentration at 1 h, which returned to pre-stress levels over a 24 h period. This was accompanied by significant upregulation of 40 genes at 1 h, and 15 genes at 24 h after stressor exposure in trout liver. Many of these genes were involved in energy metabolism, implicating a rapid liver molecular reprogramming as critical for the metabolic adjustments to an acute stressor. Several other transcripts not previously implicated in the stress response process in fish, including genes involved in immune function and protein degradative pathways, were found to be stress-responsive in trout. A large number of these stress-responsive transcripts were also shown previously to be glucocorticoid-responsive in fish. Together, our results suggest a role for stressor-mediated genomic cortisol signaling in the liver molecular programming associated with stress in fish. Overall, the study demonstrates the complex nature of the adaptive stress response at the molecular level and underscores the utility of targeted gene expression studies for identifying stress coping mechanisms.