Evolutionary adaptation and disaptation in the cold: the icefish paradigm

The aim of this chapter is to illustrate in the context of cold adaptation of the Antarctic teleosts the icefish as a unique case-study of physiological responses to genetic changes, i.e., loss of hemoglobin (Hb) and myoglobin (Mb), without apparent immediate compensatory mutations. This offers the opportunity to study the effects of epigenetic compensations and how these have been integrated at different hierarchic levels in the emergent new phenotype. However, the available evidence does not allow to clarify whether the disaptive icefish phenotype, despite its exposure to stably high environmental pO2, may have been predisposed to increased sensitivity to hypoxic disturbance (hypoxemic and intracellular hypoxia); nor to which extent this organism has been able to reprogram gene expression within aerobic tissues (including the heart), recruiting silent, alternative, or redundant pathways for correcting a deleterious, but non-lethal O2-transport phenotype. Therefore, in updating the pertinent literature, we will emphasize our view (Garofalo et al. 2009) that an inherent morpho-functional plasticity of the basic teleost cardio-circulatory system was sufficient to allow structural and functional expansion of an alternative (Hb-free blood and Mb-free cardiac muscle) design to cope with new demands. Conceivably, this disaptive condition, followed by adaptive recovery, was facilitated by the lack of competition from the comparatively sparse non-notothenioid ichthyofauna (Montgomery and Clements 2000).