Meeting Abstract
Phenotypic plasticity can either facilitate or hinder colonization of novel environments depending on whether the ancestral plastic response moves the expressed phenotype toward the environment-specific phenotypic optimum (adaptive plasticity) or away from it (maladaptive plasticity). When acclimatization responses reduce performance in a novel environment, natural selection should favor their attenuation, but the regulatory mechanisms underlying these blunted responses are poorly understood. Acclimatization responses to high elevation are well suited for exploration of both the adaptive value and mechanistic underpinnings of plastic responses because exposure to hypobaric hypoxia induces a number of physiological changes in lowland taxa. Although many of these changes are beneficial, some are maladaptive, and tend to be selected against in species that are adapted to life at high-elevation. In vertebrates, both adaptive and maladaptive physiological changes are coordinated by the hypoxia-inducible factor (HIF) signaling pathway. Here we report the finding that highland and lowland populations of deer mice exhibit extreme allele frequency variation at EPAS1, a gene that encodes the oxygen-sensitive alpha-subunit of the HIF2 transcription factor that regulates the HIF signaling cascade. We characterize phenotypic and transcriptomic changes in response to both chronic and acute hypoxia in individuals carrying alternative EPAS1 alleles, and relate them to variation in aerobic performance. Our results suggest that variation in EPAS1 may contribute to blunting of ancestral acclimatization responses that can hinder aerobic performance at high elevation (i.e. pulmonary vasoconstriction and excessive erythropoiesis), providing insight into the evolutionary modification of maladaptive plasticity.
