Meeting Abstract
In many vertebrate species, black eumelanin-based pigmentation patterns correlate with social dominance and high stress- and disease-resistance. In salmonid fishes (genus Salmo and Oncorhynchus) fish with high incidence of black melanin-based skin spots show proactive behavior, reduced post stress cortisol production, and harbour fewer ectoparasitic sea lice. Proximate molecular-genetic mechanisms for such trait associations has long remained enigmatic. Here I describe how a missense mutation in a classical pigmentation gene, melanocortin 1 receptor (MC1R), is strongly associated with distinct differences in steroidogenic melanocortin 2 receptor (MC2R) mRNA expression between genetically selected proactive (low-responsive, LR) and reactive (high responsive, HR) lines of rainbow trout (Oncorhynchus mykiss). Molecular dynamics simulation predict that melanocortin 2 receptor accessory protein (MRAP), needed for MC2R function, binds differently to the two MC1R variants. Experiments in vitro confirmed that trout MRAP interacts with the two MC1R variants and MC2R. Furthermore, mRNA for both MC1R variants and MC2R are present in head kidney cells. It would appear that genetically determined high vs low post-stress cortisol production is caused by MC2R activity being modulated in part by different binding affinities of MC1R gene variants for MRAP. We also show experimentally that exogenous cortisol increase the expression of agouti signaling protein (ASIP) mRNA in skin, which explains the association between HR-traits and reduced skin melanin patterning. Hence, skin melanisation, like immune function and a range of other traits, is modulated by the steroid hormone cortisol. The production of this hormone is in turn controlled by both environmental and genetic factors and, peculiarly, pigment genes can be found among the latter.
