Current Research Overview

      I recently completed my doctoral degree in the lab of Dr. Jay Storz at the University of Nebraska-Lincoln entitled "The Roles of Phenotypic Plasticity and Genotypic Specialization in High Altitude Adaptation" (December 2013). I am currently involved with a postdoctoral fellowship with Dr. Scott Gardner investigating the types and abundance of parasite species in pikas (Ochotona princeps and O. collaris) and marmots (Marmota flaviventris and M. caligata).

Phenotypic Plasticity of Hematological Traits

      I designed a research project to test the phenotypic plasticity of various hematological parameters in deer mice (Peromyscus maniculatus) from high and low altitude. I conducted a controlled common-garden laboratory experiment to determine whether altitude-related physiological differences were because of physiological plasticity during adulthood or developmental plasticity. This project entailed trapping deer mice using Sherman live traps and bleeding them using the maxillary vein. I measured various hemoglobin traits related to blood-O2 transport (i.e. Hemoglobin concentration ([Hb]), Hematocrit (Hct), red cell count, red cell size, mean cell Hb concentration (MCHC), and allosteric effector concentration ([DPG]), etc.). Mice were kept in a common-garden low altitude environment for 6 weeks and then bled again. I also tested the F1 generation mice from high or low altitude parental crosses. I found that in their native habitats high altitude deer mice have a higher [Hb], Hct, and [DPG], but lower MCHC and smaller red cells than low altitude mice. However, these differences disappear after acclimatization to normoxia at low altitude. These differences are not due to developmental plasticity because F1 descendants of both high and low altitude were indistinguishable.

      As a follow-up to this experiment, I performed the reciprocal experiment where F1 descendants of either high or low altitude parents were born and raised in a low altitude common-garden environment and then allowed to acclimate to hypoxia for 6 weeks using hypobaric chambers. These mice were bled before and after hypoxia acclimation and mostly the same hematological traits were measured. From this research I was able to determine that the traits I measured were environmentally induced, except with RBC size which may be constrained by genetic control. High and low altitude descendants both increased oxygen carrying capacity in hypoxia, however the low altitude F1 mice increased the number and size of RBCs more than the high altitude F1 mice. This may result in a disadvantage to the low altitude mice because of an increase in the cost of pumping more viscous blood.

Variation in Mammalian Hemoglobin Function 

     I designed a research project to examine blood-O2 affinity in pikas (Ochotona spp.) and marmots (Marmota spp.). Elevated O2 affinity has been observed in many organisms that reside in hypoxic high altitude environments. Adjustments in blood-O2 affinity may be from structural changes in Hb amino acid mutations that increase intrinsic O2-affinity of the tetramer and/or mutations that may suppress the sensitivity of Hb to inhibitory effects of allosteric effectors within erythrocytes. I sequenced the alpha and beta Hb genes of two closely related pika (O. princeps and O. collaris) and marmot (M. flaviventris and M. caligata) species with different altitudinal distributions to identify posible amino acid substitution(s) that may be responsible for observed functional differences. I also measured the O2-binding properties of purified Hbs and its response to various allosteric effectors (DPG, Cl-). For the marmots, I found that there was no difference in the response of the two species to allosteric effectors. For the pikas, I discovered that the high altitude (O. princeps) species has a higher Hb-O2 affinity in the presence and absence of allosteric effectors and this is exclusively attributable to intrinsic differences between the two species. From alpha- and beta-globin sequence analysis I found a few candidate residue mutations (alpha78, and beta5, 58, 62, 123, 126) that may be responsible for an increase in O2 affinity in the high altitude pika. Using the mutations in the beta-globin gene I constructed recombinant Hb (rHb) mutants using site directed mutagenesis to mimic the genotypes of O. princeps, O. collaris, and their most recent common ancestor. I found that O. princeps had a higher Hb-O2 affinity in the presence and absence of allosteric effectors (DPG, Cl-) than both O. collaris and the inferred ancestor meaning that this is a derived character state. This process allowed me to infer which substitutions lead to the increased affinity in O. princeps and to better understand the pleiotropic and epistatic interactions between these substitutions. 

Side Projects 


Harold W. Manter Parasitology Lab

        I performed necropsies on pika and marmot individuals collected from Colorado and Alaska. I identified and preserved all parasite species collected using various methods (i.e. preserving specimens in different concentrations of ethanol, formalin, and various techniques for mounting specimens). I am also helping to establishing a molecular parasitology lab where we will be sequencing various genes (i.e. COI, cyt-b, 16S, etc.) and using molecular data instead of only morphological characteristics to resolve phylogenetic lineages of parasites.

Internship in the Conservation Genetics Lab at the Henry Doorly Zoo

      I am currently working in the Molecular Genetics Department on a project using non-invasive genetic techniques to determine the population structure of the Greater Bamboo Lemur (Prolemur simus) in Madagascar. I am also working on the Madagascar Biodiversity Project (MBP) using microsatallite nuclear DNA markers to determine differences in lemur distribution and species.

Past Research 

Fire Ant Research

     I worked with the invasive red imported fire ant (Solenopsis invicta) and different biological control agents (i.e. bacteria and viruses) to try and reduce S. invicta population sizes in east Texas.  One of our main goals was to find a suitable biological control agent to induce colony collapse disorder (CCD) among S. invicta colonies. We characterized the type of bacteria within the ant's hemolymph and the ovaries of queens to determine what type of bacteria was present and how it was transferred within a colony. We also investigated the Solenopsis invicta virus 1 (SINV-1) and its potential to cause CCD. I discovered a new variant and named it SINV-TX5. I also devised new techniques for extracting, microencapsulating, and delivering virus to uninfected colonies. We conducted another experiment using commonly used, commercially available pesticides in the presence/absence of SINV. We hypothesized that the virus would weaken the ant's immune system allowing the pesticides to be more effective and increasing colony mortality. Surprisingly, we discovered that SINV actually provides some type of protection to individuals protecting them from mortality.

Flying Squirrel Research

     I conducted research on the evolutionary relationship between two populations of southern flying squirrel (Glaucomys volans) separated by many man-made geographic barriers in east Texas. I collected ear clippings from a total of 43 squirrels and used mitochondrial DNA (mtDNA) genes (i.e. cytochrome b and control region). I used several tree-building programs to construct a phylogeny between the two populations (e.g. Mesquite, TNT, MEGA). I determined that the two populations are experiencing an expansion event. It is likely that at one point this was one continuous population and the habitat reduction resulted in a bottleneck effect and rapid population decline.

Wildlife Population Genetics Research

     I was involved in developing microsatellite markers for Swainson's hawks (Buteo swainsoni) and other Buteo spp. to determine the population structure and genetic diversity of this genus. 

Population Genetics Research

     I performed multiple experiments involving fruit flies (Drosophila spp.) as our model organism. In one project we identified the genes responsible for the QTL divergence of sex-comb tooth number between two species of Drosophila. I also designed a research project to investigate at what stage in development changes in gene expression are likely to result in changes in phenotype. We examined the contributions maternal genes provided to genetic variation and the contributions upstream genes confer to downstream target genes in two different gene regulatory networks (GNRs).

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