Timothy Allen Evans

Timothy Allen Evans

Assoc Professor

J. William Fulbright College of Arts & Sciences

(BISC)-Biological Sciences

Phone: 479-575-3220

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My laboratory is primarily a developmental genetics laboratory, and we study the development of the insect central nervous system (CNS) using the model species Drosophila melanogaster (the fruit fly) and Tribolium castaneum (the flour beetle). We use a variety of approaches spanning genetics, molecular biology, cell biology, and biochemistry to investigate how the insect nervous system is properly wired during embryonic development. Our primary focus is on axon guidance, the process by which neurons extend membrane processes (axons) across long distances in search of the target cells with which they will form the cell-cell connections (synapses) necessary for the proper functioning of the nervous system. Our research focuses on the roles of the midline repellant ligand Slit and its Roundabout (Robo) receptors in midline crossing and axon pathway formation in Drosophila and Tribolium. 

The Slit/Robo signaling pathway controls a number of fundamental axon guidance decisions in invertebrates and vertebrates alike. Flies and beetles, like mice and humans, each possess a number of different Robo receptor genes, and each Robo family member plays a unique set of roles in axon guidance. By studying the diverse roles of the Robo receptor family in Drosophila, and by comparing the functions of Robo receptors across different animal species, we hope to learn how a limited number of molecules specify the diverse axon guidance outcomes necessary for proper nervous system connectivity, and how axon guidance mechanisms have changed over evolutionary time.

BIOL2323 General Genetics (Fall)

Comparative Neurobiology (Spring)

B.S. Biology, Slippery Rock University of Pennsylvania, 2001

Ph.D. Genetics, Indiana University, 2006

Post-doc, University of Pennsylvania, 2006-2013

Evans, T.A. (2017). CRISPR-based gene replacement reveals evolutionarily conserved axon guidance functions of Drosophila Robo3 and Tribolium Robo2/3. EvoDevo 8:10. doi:10.1186/s13227-017-0073-y.

Evans, T.A. (2016). Embryonic axon guidance: insights from Drosophila and other insects. Curr. Opin. Insect Sci. 18: 11-16. doi:10.1016/j.cois.2016.08.007.

Reichert, M.C., Brown, H.E., and Evans, T.A. (2016). In vivo functional analysis of Drosophila Robo1 immunoglobulin-like domains. Neural Dev. 11(1):15. doi:10.1186/s13064-016-0071-0.

Brown, H.E., Reichert, M.C., and Evans, T.A. (2015). Slit binding via the Ig1 domain is essential for midline repulsion by Drosophila Robo1 but dispensable for receptor expression, localization and regulation in vivo. G3 (Bethesda) 5(11):2429-39. doi:10.1534/g3.115.022327.

Evans, T.A.*, Santiago, C.*, Arbeille, E., and Bashaw, G.J. (2015). Robo2 acts in trans to inhibit Slit-Robo1 repulsion in pre-crossing commissural axons. eLife 4:e08407. *equal contribution. doi:10.7554/eLife.08407.

Evans, T.A. and Bashaw, G.J. (2012). Slit/Robo-mediated axon guidance in Tribolium and Drosophila: divergent genetic programs build insect nervous systems. Dev. Biol. 363: 266-278. doi:10.1016/j.ydbio.2011.12.046.

Evans, T.A. and Bashaw, G.J. (2010). Functional diversity of Robo receptor immunoglobulin domains promotes distinct axon guidance decisions. Curr. Biol. 20: 567-572. doi:10.1016/j.cub.2010.02.021.

Evans, T.A. and Bashaw, G.J. (2010). Axon guidance at the midline: of mice and flies. Curr. Opin. Neurobiol. 20: 79-85. doi:10.1016/j.conb.2009.12.006.

Evans, T.A., Haridas, H. and Duffy, J.B. (2009). Kekkon5 is an extracellular regulator of BMP signaling. Dev. Biol. 326(1):36-46. doi:10.1016/j.ydbio.2008.10.002.

Alvarado, D., Evans, T.A., Sharma, R., Lemmon, M.A. and Duffy, J.B. (2006). Argos mutants define an affinity threshold for Spitz inhibition in vivo. J. Biol. Chem. 281(39):28993-29001. doi:10.1074/jbc.M603782200.

MacLaren, C.M.*, Evans, T.A.*, Alvarado, D.* and Duffy, J.B. (2004). Comparative analysis of the Kekkon molecules, related members of the LIG superfamily. Dev. Genes Evol. 214(7):360-6. *equal contribution. doi:10.1007/s00427-004-0414-4.