Northwest Labs B103
Speaker: Miriam Goodman (Stanford)
Abstract: Touch is the first sense to develop, the last to fade and the least well understood of the five basic senses. We have long 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 channels remained elusive for decades. Research in my group and others has identified at least four classes of proteins that can form these so-called mechanoelectrical transduction (MeT) channels in mammals and invertebrates: DEG/ENaC/ASIC sodium channels, TMC cation channels, TRP cation channels, and Piezo cation channels. Although other classes of force-sensitive channels are being discovered, their role in sensation is not yet known. The DEG/ENaC/ASIC and TMC channels are thought to activate through a force-from-filament activation mode, while the others operate in a force-from-lipid mode. Regardless of which force-dependent gating model applies, we hypothesize that the subcellular position of MeT channels is tightly regulated and helps to determine the threshold and dynamic range of touch sensation (Sanzeni et al, eLife, 2019; Katta et al, J Gen Physiol, 2019). Work in our research group integrates genetic dissection with cellular biophysics, molecular imaging, and techniques for controlled delivery of force its effect on ion channel activity and cellular tension. We focus on the touch receptor neurons in C. elegans as an ideal platform for integrating studies at the molecular, cellular, and behavioral levels. This talk will discuss evidence supporting the view that touch sensitivity depends on the molecular architecture the sensory neuron-skin cell interface and present new work identifying the protein partners that determine and maintain MeT position.