Ashlee H. Rowe, PhD
Assistant Professor, Zoology
Ph.D., 2004, North Carolina State University
Office Address: 432 Giltner
Office Phone: 517-432-4468
Broadly, I am interested in sensory and motor systems and their role in the evolution of adaptive behavior, particularly traits that mediate interactions between animals. My ultimate goal is to understand how animals adapt to their environment. My research program is integrative and focuses on understanding the biochemical, molecular, genetic and physiological bases of adaptive behavior. To address these questions, I study traits that are at the interface of species interactions. Currently, I am investigating the evolution of scorpion neurotoxins and their targets, ion channels and receptors expressed in nerve and muscle tissue. Scorpions employ complex mixtures of toxins as chemical weapons to subdue their prey and defend themselves against their predators and competitors. Neurotoxins that induce pain, paralysis, seizures and death impose strong selection on the receivers, thus driving the evolution of adaptations that mediate interactions between the scorpions and their enemies.
Currently, I am investigating the sensory neurobiology of pain-inducing neurotoxins and their targets, sodium (Na+) and potassium (K+) ion channels expressed in dorsal root ganglion (DRG) neurons (nociceptors) that regulate pain sensation. The system I study includes a genus of scorpions (bark scorpions, Centruroides spp.) that produce multiple neurotoxins that selectively bind Na+ and K+ ion channels expressed in nerve and muscle tissue, and a group of their predators (grasshopper mice, a.k.a. scorpion mice, Onychomys spp.) that have evolved resistance to the neurotoxins. The evolution of pain-inducing neurotoxins in bark scorpions and pain resistance in their predators provides an ideal system for studying adaptive behavior at the biochemical, molecular, genetic and physiological levels. Interactions between scorpions and mice can be studied in both natural habitats and under controlled conditions in the laboratory. Bark scorpion neurotoxins can be isolated using biochemical techniques, screened for pain-inducing capability using a behavioral assay, and their ion channel targets identified using electrophysiological recordings from both native channels expressed in nerve cells and heterologously-expressed channels. Because bark scorpion neurotoxins act as specific environmental stimuli that select for specific variants of genes encoding Na+ and K+ ion channels expressed in grasshopper mice, I can use cloning and sequencing techniques coupled with site-directed mutagenesis and an expression system to quantitatively assess the functional consequences of structurally modified ion-channel targets in grasshopper mice. Moreover, I can measure the fitness consequences and physiological tradeoffs associated with toxin resistance in the mice.
Interactions between neurotoxins and their ion channel targets also provide an excellent opportunity to test hypotheses aimed at understanding coevolutionary processes, i.e., “arms races” in which the evolution of one species drives and is driven by the evolution of another species. Because both scorpion neurotoxins and their ion-channel targets are the products of gene families, this system provides the opportunity to study coevolution at the molecular genetic and genomic levels.
- Rowe, A.H., Xiao, Y., Rowe, M.P., Cummins, T.R., and Zakon, H.H. (2013) Voltage-gated sodium channel in grasshopper mice defends against bark scorpion toxin. Science, in press.
- Rowe, A.H., Xiao, Y., Scales, J., Linse, K.D., Rowe, M.P., Cummins, T.R. and Zakon, H.H. (2011) Isolation and characterization of CvIV4: a pain-inducing -scorpion toxin. PLoS ONE 6(8): e23520. doi:10.1371/journal.pone.0023520
- Rowe, A.H. and Rowe, M.P. (2008) Physiological resistance of grasshopper mice (Onychomys spp.) to Arizona bark scorpion (Centruroides exilicauda) venom. Toxicon 52:597-605.
- Rowe, A.H. and Rowe, M.P. (2006) Risk assessment by grasshopper mice (Onychomys spp.) feeding on neurotoxic prey (Centruroides spp.). Animal Behaviour 71:725-734.
- Luckenbach, J.A., Early, L.W., Rowe, A.H., Borski, R.J., Daniels, H.V. and Godwin, J. (2005) Aromatase cytochrome P450: cloning, intron variation, and ontogeny of gene expression in southern flounder (Paralichthys lethostigma). Journal of Experimental Zoology 303A:643-656.
- Lyons, D., Miller, M., Rowe, A.H., Crane, A.M. and Porrino, L.J. (1998) Time-dependent effects of acute ethanol administration on regional cerebral blood flow in the rat. Alcohol 16:213-219.
- Daunais, J.B., Hart, S.L., Hedgecock, A.A., Matasi, J.J., Thornley, C., Davies, H.M.L. and Porrino, L.J. (1997) Alterations in behavior and opioid gene expression induced by the novel tropane analog, WF-31. Molecular Brain Research 50:293-304.
- Letchworth, S.R., Daunais, J.B., Hedgecock, A.A. and Porrino, L.J. (1997) Effects of chronic cocaine administration on dopamine transporter mRNA and protein in the rat. Brain Research 750:214-222.
- Porrino, L.J., Miller, M., Hedgecock, A.A., Thornley, C., Matasi, J.J. and Davies H.M.L. (1997) Local cerebral metabolic effects of the novel cocaine analog, WF-31: comparisons to fluoxetine. Synapse 27:26-35.