As of April 2017, I’ve been accepted as an NIH postdoctoral fellow at the University of Montana! My project will explore the physiological and fitness consequences of selection on Epas1, a master regulator of the body’s response to hypoxia. This gene is under strong natural selection in highland populations of deer mice, as well as humans, wolves, and many other mammals native to high-elevations.
Here is how this project is relevant to the NIHs goals:
The disruption of oxygen homeostasis is a crucial feature in the pathophysiology of many common and devastating diseases, including heart disease, chronic lung disease, and cerebrovascular disease. Populations (e.g., highland Tibetan humans) that have adapted to high-altitude environments are protected from the negative effects of extremely low oxygen availability (hypoxia), in part because they have modified a key hypoxia-signaling pathway known as the hypoxia-inducible factor (HIF) cascade. I propose to use deer mice (Peromyscus maniculatus), which have naturally adapted to high-altitude, as a model to determine the molecular and genetic mechanisms by which heart, lung, and blood responses to hypoxia benefit from Darwinian selection on the HIF cascade. A mechanistic understanding of adaptation to hypoxia will yield insight into novel therapies in the treatment of diseases related to the loss of oxygen homeostasis.