Deciphering Touch Sensation and Neuronal Mechanoprotection
Monday, March 26, 2018 - 12:00pm
Joseph Henry Room, Jadwin Hall
CUNY-Princeton Biophysics Seminar
Physics and the Lewis-Sigler Institute

Touch is the first sense to develop, the last to fade and the least well understood of the five basic senses. For decades, we have understood that ion channels were the first responders of touch sensation—converting the mechanical energy delivered in a touch or the bend of a limb into neural signals. Yet, the identity of the proteins forming such proteins remained elusive. Research in my group and others has identified at least three classes of proteins that can form these so-called mechanoelectrical transduction (MeT) channels in mammals and invertebrates—DEG/ENaC sodium channels, TRP cation channels, and Piezo cation channels. We are working to expand our knowledge of how MeT channels depend on biophysics of force transfer for activation (Eastwood et al, PNAS 2015) and continuing to investigate the protein partners that make these channels. My talk will survey prior knowledge and discuss our recent investigations applying the tools of genetic dissection to the biophysics of in vivo MeT channel activation using C. elegans nematodes as a tractable model.
The sensory neurons responsible for the sense of touch and proprioception invade the skin, muscles, and joint. By virtue of their anatomical position, they experience persistent and potentially damaging mechanical stresses. Yet, sensory neurons are remarkably resilient to such stresses. Recently, we identified a key role for pre-stress in actin-spectrin networks in the mechanical resilience of sensory neurons and deployed novel genetically-encoded indicators of mechanical strain (Krieg et al, 2014, Nat Cell Biol; Krieg et al, 2017 e Life). I will discuss on-going work involving physical models for mechanical stability based on twist-tension coupling in axons and genetic dissection to identify hothe cytoskeleton is fundamental to neuronal mechanoprotection.