The Roles of Phenotypic Plasticity and Genotypic Specialization in High Altitude Adaptation

Authors

Danielle M. Tufts, University of Nebraska-LincolnFollow

Date of this Version

Fall 12-2013

Document Type

Article

Citation

Tufts, Danielle M. (2013). The Roles of Phenotypic Plasticity and Genotypic Specialization in High Altitude Adaptation. PhD dissertation, University of Nebraska-Lincoln.

Comments

A DISSERTATION Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Doctor of Philosophy, Major: Biological Sciences (Ecology, Evolution, and Behavior), Under the Supervision of Professor Jay F. Storz. Lincoln, Nebraska: December, 2013

Copyright (c) 2013 Danielle M. Tufts

The first chapter of this dissertation has been published in the Journal of Experimental Biology (2013) 216(7):1167-73.

Abstract

In vertebrates living at high altitude, arterial hypoxemia may be ameliorated by reversible changes in the oxygen-carrying capacity of the blood (regulated by erythropoiesis) and/or changes in blood–oxygen affinity (regulated by allosteric effectors of hemoglobin function). These hematological traits often differ between taxa that are native to different elevational zones, but it is often unknown whether the observed physiological differences reflect fixed, genetically based differences or environmentally induced acclimatization responses (phenotypic plasticity). Here, we report measurements of hematological traits related to blood–O₂ transport in populations of deer mice (Peromyscus maniculatus) that are native to high- and low-altitude environments. We conducted a common-garden breeding experiment to assess whether altitude-related physiological differences were attributable to developmental plasticity and/or physiological plasticity during adulthood. Under conditions prevailing in their native habitats, high-altitude deer mice from the Rocky Mountains exhibited a number of pronounced hematological differences relative to low-altitude conspecifics from the Great Plains. However, these differences disappeared after 6 weeks of acclimation to normoxia at low altitude. These results indicate that the naturally occurring hematological differences between highland and lowland mice are environmentally induced and are largely attributable to physiological plasticity during adulthood. The reciprocal experiment in which highland and lowland natives were subjected to 6 weeks of chronic hypoxia revealed that highland mice may have evolved a blunted erythropoietic response to chronic hypoxia.

As an alternative to plastic responses, genetically based changes in the respiratory properties of hemoglobin can also contribute to hypoxia adaptation in high-altitude vertebrates. Under severe hypoxia, an increase in hemoglobin-O₂ affinity can help preserve an adequate level of tissue oxygenation by enhancing pulmonary O₂ uptake while simultaneously maintaining the pressure gradient that drives O₂ diffusion from capillary blood to the tissue mitochondria. In comparisons between high- and low-altitude species of pikas (Ochotona princeps and O. collaris, respectively), we demonstrated that the high-altitude species has evolved a derived increase in hemoglobin-O₂ affinity. Using ancestral sequence reconstruction and site-directed mutagenesis, we identified a set of three β-chain substitutions that are responsible for the evolved change in hemoglobin function.

Advisor: Jay F. Storz