Ashlee Rowe
AssociateProfessor, Biological Sciences Richards Hall 207, 309, & 310 405-325-5465 ahrowe at ou dot edu Ph.D., Zoology (Genetics, Behavior) - North Carolina State University, 2004RESEARCH:
How do changes in gene structure and expression produce physiological changes that underlie complex behaviors? My lab addresses this question by investigating the molecular and physiological mechanisms of sensory and neuromuscular adaptations underlying predatory behavior (risk assessment, prey choice, prey-specific attack behavior, adaptation to prey defenses, learning, aversive conditioning). We study predator-prey interactions because they rely on fast, specialized sensory inputs and neuromuscular responses, and we focus on ion channels because they encode sensory information and regulate responses to stimuli. Interactions between carnivorous mice (grasshopper mice) and their chemically-defended prey (scorpions, centipedes, tarantulas, darkling beetles) provide a powerful, ecologically relevant model for examining the role of ion channels in adaptations that mediate predatory behavior. Scorpions, centipedes, tarantulas and darkling beetles produce complex mixtures of neurotoxins (peptides, chemicals) that bind ion channels in sensory and neuromuscular systems, disrupting neuronal signaling and muscle contraction. Toxins that target ion channels (Na+, K+, TRP) in sensory systems induce burning pain and sensitivity to touch, while toxins that target channels in motor neurons and skeletal muscle cause paralysis, seizures and death. Pain and death impose strong selection on predators, thus driving the evolution of adaptations that mediate interactions between chemically-defended arthropods and their enemies. For example, grasshopper mice have evolved resistance to multiple toxins via changes to ion channels in their sensory and motor neurons, and skeletal muscle. Current projects aim to 1) characterize peptides and chemicals that target ion channels; 2) determine how changes in the structure, function and expression of channels impart toxin resistance to predators; 3) determine how modifications to sensory and neuromuscular systems shape predatory behavior. Our system is highly tractable because we study interactions between grasshopper mice and their prey in both natural habitats and the laboratory. We use biochemistry to isolate peptides and chemicals, and then combine electrophysiology of ion channels and tissues with behavioral analyses to characterize the effects of toxins on sensory and neuromuscular systems. Because toxins act as stimuli that select for variants of genes encoding ion channels in grasshopper mice, we use cloning, site-directed mutagenesis and an expression system to assess the functional consequences of structurally modified channels. Moreover, we can measure the fitness consequences and physiological tradeoffs associated with toxin resistance.
Selected Publications:
Perez Callez, C., Lilue, J., Anderson, E., Haggerty, L., Martin, F. J., McCarthy, S. A., Adams, D. J., Thybert, D., Rowe, A. H., and Keane, T. M. (2026) The Onychomys pangenome reveals the unique molecular adaptations that confer toxin resistance. Genome Biology, in press.
Marske, K. A., Lanier, H. C., Siler, C. D., Rowe, A. H., and Stein, L. (2023) Integrating biogeography and behavioral ecology to rapidly address biodiversity loss. PNAS 120: 1-10.
Al-Sabi, A., Mohamed Abd El-Aziz, T., Yu, P., Rowe, A. H., and Wulff, H. (2022) Editorial: Ion channels in health and disease. Frontiers in Physiology: Membrane Physiology and Membrane Biophysics 13: 1093210.
George, K., Lopez-Mateos, D., Mohamed Abd El-Aziz, T., Xiao, Y., Kline, J., Bao, H., Raza, S., Stockand, J. D., Cummins, T. R., Fornelli, L., Rowe, M. P., Yarov-Yarovoy, V., and Rowe, A. H. (2022) Structural and functional characterization of a novel scorpion toxin that inhibits Nav1.8 via interactions with the DI voltage sensor and DII pore module. Frontiers in Pharmacology: Pharmacology of Ion Channels and Channelopathies 13: 846992.
Mohamed, T. A. E., Xiao, Y., Kline, J., Gridley, H., Heaston, A., Linse, K. D., Ward, M. J., Rokyta, D. R., Stockand, J. D., Cummins, T. R., Fornelli, L. and Rowe, A. H. (2021) Identification and characterization of novel proteins from Arizona bark scorpion venom that inhibit Nav1.8, a voltage-gated sodium channel regulator of pain signaling. Toxins 13: (501) 1-21.
Niermann, C. N., Tate, T. G., Suto, A. L., Barajas, R., White, H. A., Guswiler, O. D., Secor, S. M., Rowe, A. H. and Rowe, M. P. (2020) Defensive venoms: is pain sufficient for predator deterrence? Toxins 12: (260) 1-17.
Carcamo-Noriega, E. N., Olamendi-Portugal, T., Restano-Cassulini, R., Rowe, A., Uribe-Romero, S. J., Becerril, B., and Possani, L. D. (2018) Intraspecific variation of Centruroides sculpturatus scorpion venom from two regions of Arizona. Arch. Biochem. Biophys. 638: 52-57.
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 342(6157): 441-446.
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 α-scorpion toxin. PLoS One 6(8): e23520.
Rowe, A. H. and Rowe, M. P. (2008) Physiological resistance of grasshopper mice (Onychomys spp.) to Arizona bark scorpion (Centruroides exilicauda) venom. Toxicon 52(5): 597-605.