- B.A., Biology, Carleton College, Northfield, MN (1990)
- Ph.D., Neuroscience, Washington University School of Medicine, St. Louis, MO (1996)
- Postdoctoral Fellow, Stanford University, Department of Molecular and Cellular Physiology and HHMI, (1996-1997)
- Stanford University, Howard Hughes Medical Institute
I began my career as a neuroscientist at the Whitney Marine Laboratory of the University of Florida as an NSF REU fellow during my Junior year in college, where I studied electrical coupling of cells in the retina. I went on to study ion channel evolution under Dr. Larry Salkoff at Washington University in St. Louis in graduate school. I wrote a paper on the subject in an undergraduate evolution class, and Larry gave me the opportunity to begin to address some of the open questions for my graduate thesis. I move on to do postdoctoral work on the diversity and function of large-conductance calcium-activated (BK) channels in Dr. Richard Aldrich’s lab at Stanford. I then spent 8 years working on ion channels as drug targets in industry, before returning to academics to explore the functional roles of newly discovered K+ channels in neuronal signaling. We are interested in how these channels control firing threshold and how they make neural circuits seizure resistant. At Penn State, I have also returned to my evolutionary roots to explore how neuronal signaling evolved at genomic, molecular and cellular levels. We use a new cnidarian model organism Nematostella vectensis for much of this work. I am particularly interested in using the lab's research mission to provide opportunities for undergraduate and graduate research training.
My main interest is to understand how neuronal excitability is controlled on a cellular and molecular level and how it evolved. Neuronal electrical signals are generated by ion channels and shaped by the structure of the neuron itself. We study the functional evolution of the major neuronal ion channel gene families in order to better understand how they pattern the activity of neurons and circuits. The lab focuses on ion channels that initiate sensory signals and control firing threshold. How did these channels evolve, and what can evolutionary conservation tell us about their function and regulation? We are also interested how the structural polarity of neurons evolved as it relates to directional signaling and ion channel distribution. We aim to gain fundamental insights into how polar neurons are built by identifying key features conserved through evolution.
Please visit our lab website for information about current projects.
A major diversification of voltage-gated K+ channels occurred in ancestral parahoxozoans. Xiaofan Li, Hansi Liu, Jose Chu Luo, Sarah A. Rhodes, Liana M. Trigg, Damian B. van Rossum, Andriy Anishkin, Fortunay H. Diatta, Jessica K. Sassic, David K. Simmons, Bishoy Kamel, Monica Medina, Mark Q. Martindale, and Timothy Jegla (2015) Proc Natl Acad Sci USA, In Press.
Ether-a-go-go family Voltage-Gated K+ Channels evolved in an ancestral metazoan and functionally diversified in a Cnidarian/Bilaterian Ancestor. Li X., Martinson A.S., Layden M.J., Diatta F.H., Sberna A.P., Simmons D.K., Martindale M.Q., Jegla T. (2015) J Exp Biol, In press.
Neuronal polarity: an evolutionary perspective. Melissa M. Rolls and Timothy J. Jegla (2015) J Exp Biol., In press.
Functional evolution of Erg potassium channel gating reveals an ancient origin for IKr. Martinson A.S., van Rossum D.B., Diatta F.H., Layden M.J., Rhodes S.A., Martindale M.Q., Jegla T. (2014) Proc Natl Acad Sci USA. 15;111(15):5712-7. PMCID: PMC3992637.
External pH modulates EAG superfamily K+ channels through EAG-specific acidic residues in the voltage sensor. Kazmierczak M, Zhang X, Chen B, Mulkey DK, Shi Y, Wagner PG, Pivaroff-Ward K, Sassic JK, Bayliss DA, Jegla T (2013) 2013. J Gen Physiol. Jun; 141(6):721-35. PMCID: PMC3664700.
Expanded functional diversity of Shaker K+ channels in cnidarians is driven by gene expansion. Jegla T, Marlow HQ, Chen B, Simmons DK, Jacobo SM, Martindale MQ. (2012) PLoS One. 2012;7(12):e51366. PMC3519636.
Spiroindolones, a potent compound class for the treatment of malaria. Rottmann M, McNamara C, Yeung BK, Lee MC, Zou B, Russell B, Seitz P, Plouffe DM, Dharia NV, Tan J, Cohen SB, Spencer KR, González-Páez GE, Lakshminarayana SB, Goh A, Suwanarusk R, Jegla T, Schmitt EK, Beck HP, Brun R, Nosten F, Renia L, Dartois V, Keller TH, Fidock DA, Winzeler EA, Diagana TT. (2010) Science. 2010 Sep 3;329(5996):1175-80.
Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy. Zhang X., Bertaso F., Yoo J., Baumgartel K., Clancy S.M., Lee V., Cienfuegos C., Wilmot C., Avis J., Huynh T., Daguia C., Schmedt C., Noebels J., Jegla T. (2010) Nat Neurosci. 2010 Sep;13(9):1056-8.
Divalent cations slow activation of EAG family K+ channels through direct binding to S4. Zhang, X., Bursulaya, B., Lee, C., Chen, B, Pivaroff, K., Jegla, T. (2009) Biophys J. Jul 8;97(1):110-20.
Evolution of the Human Ion Channel Set. Jegla, T., Zmasek, C., Batalov, S., Nayak, S.K. (2009) Combinatorial Chemistry & High Throughput Screening. Jan;12(1):2-23.
An internal thermal sensor controlling temperature preference in Drosophila. Hamada F.N., Rosenzweig M., Kang K., Pulver S.R., Ghezzi A., Jegla T.J. Garrity P.A. (2008) Nature. 10;454(7201):217-20.
Illumination of the melanopsin signaling pathway. Panda S., Nayak S., Campo B., Hogenesch J., Jegla, T. (2005) Science 307(5709):600-604.
A TRP-like channel expressed in nociceptive neurons, is activated by cold temperatures. Story G.M., Peier A.M., Reeve A.J., Eid S.R., Mosbacher J., Hricik T.R., Earley T.J., Hergarden A.C., Andersson D.A., Hwang S.W., McIntyre P., Jegla T., Bevan S., Patapoutian A. (2003) ANKTM1, Cell 112(6):819-29.
Opposite thermosensor in fruitfly and mouse. Viswanath V, Story GM, Peier AM, Petrus MJ, Lee VM, Hwang SW, Patapoutian A, Jegla T. (2003) Nature. 2003 Jun 19;423(6942):822-3.