After receiving his B.S. in Cell and Molecular Biology at Texas Tech University, Richard Walker (walkerri@ohsu.edu) received his Ph.D. in Neuroscience in 1995 from the University of Texas Southwestern Medical Center. He then trained as a post-doctoral fellow at the University of California, San Diego. In 2000 Walker was appointed as an assistant professor to the Oregon Hearing Research Center with a joint appointment in the Vollum Institute. Click here to see Prof. Walker's page at the OHSU Neuroscience graduate school.

The umbrella of mechanical senses covers a diverse set of sensory modalities, including touch, hearing, balance, and proprioception. While very different cells perform the task of collecting information about the mechanical world for each mechanosensory system, they all appear to do it in the same way: directly converting energy in a mechanical stimulus, be it whisper or a hammer blow to your thumb, to an electrical signal that is passed on to the central nervous system. How, then, do sensory cells transduce mechanical stimuli into electrical signals? To answer this question, research in our lab takes advantage of the ease and elegance of Drosophila research and can be divided into two parts: a molecular-genetic path to identify the genes involved in mechanosensory transduction and an electrophysiological approach to understanding both wild-type and mutant mechanosensory responses. While each of these approaches is powerful in its own right, combining them gives a comprehensive set of tools both to identify the molecules of mechanosensation and to show how they work together converting mechanical stimuli into electrical signals.

We recently identified a Drosophila mechanosensory transduction channel, called NompC, that mediates about 90% of the mechanotransduction current. The cloning of a NompC represents the first peek into the molecules that make up the transduction machinery in flies. Using NompC as a toehold into the transduction cascade gives us a tremendous advantage over traditional genetic screens: the proteins that interact with NompC either genetically or biochemically can now be precisely targeted. While identifying other transduction components will be necessary to comprehend mechanosensation, an in-depth understanding will require a great deal more biophysical experimentation, particularly on isolated mechanosensory neurons. We are therefore developing an isolated-cell preparation to record whole-cell, voltage-clamped transduction currents. This preparation will allow simultaneous manipulation of both the interior and exterior of the mechanoreceptor neuron and its transduction machinery. This precise control will be key to the identification of transduction molecules and understanding how they transform a mechanical force into electrical information.

Gillespie, P.G. and Walker,(2001) R. G. Molecular basis of mechanosensory transduction. Nature. 413:194-202.

Walker, R. G., Willingham, A. T., and Zuker, C. S. (2000) A Drosophila mechanosensory transduction channel. Science 287:2229-2234.

Barolo, S. Walker, R. G., Polyanovsky, A. D., Freschi, G., Keil, T., and Posakony, J. W. (2000) A novel notch-independent activity of Suppressor of Hairless is required for normal mechanoreceptor physiology. Cell 103:957-969.

Walker, R. G. and Hudspeth, A. J. (1996) Calmodulin controls adaptation of mechanoelectrical transduction by hair cells of the bullfrog’s sacculus. Proc. Natl. Acad. Sci. USA. 93: 2203-2207.

Walker, R. G., Hudspeth, A. J., and Gillespie, P. G. (1993) Calmodulin and calmodulin-binding proteins in hair bundles. Proc. Natl. Acad. Sci. USA. 90: 2807-2811.