Ectothermy and endothermy: evolutionary perspectives of thermoprotection by HSPs

Living organisms respond to heat exposure by selectively expressing heat shock proteins (HSPs). Accumulation of HSPs confers thermotolerance in cell cultures and in ectotherms and is an important component of the heat shock response. This response, however, has not been directly examined in relation to different ;thermal states', namely ectothermy vs endothermy. By using avian development as a model system for transition from ectothermy to endothermy, we show that, in contrast to the ectothermic state, in the endothermic state the organism is more resistant to heat but relies less on HSPs as a first-line thermoprotective mechanism. Moreover, intraspecific, real-time, in vivo measurements in genetically diverse fowl strains relate improvement of thermoresistance in endotherms to improved body temperature (Tb) regulation, with a concomitant delay in the expression of HSPs. The time course of this delay and the Tb at which it occurs imply that the ontogenetic and evolutionary pathways leading to improved thermoresistance may have followed two, apparently non-related, parallel routes--cellular and peripheral (non-cellular). In search of other cellular components that differentially participate in the heat shock response, we revealed a significant expression of fatty acid synthase (FAS) in heat-exposed endotherms but not in ectotherms.