Professor Stephen Rogers
University of North Carolina at Chapel Hill
Friday, March 22, 2019 - 11:00am
Ramsay Wright Building, Room 432
At the cellular level, α-tubulin acetylation alters the structure of microtubules to render them mechanically resistant to compressive forces. How this biochemical property of microtubule acetylation relates to mechanosensation remains unknown, though prior studies have shown that microtubule acetylation plays a role in touch perception. Here, we identify the major Drosophila α-tubulin acetylase (dTAT) and show that it plays key roles in several forms of mechanosensation while exerting little effect on other sensory modalities. dTAT is highly expressed in neurons of the larval peripheral nervous system (PNS) but is not required for normal neuronal morphogenesis. We show that mutation of the acetylase gene or the K40 acetylation site in α-tubulin impairs mechanical sensitivity in sensory neurons and behavioral responses to gentle touch, harsh touch, gravity, and sound stimulus, but not thermal stimulus. Finally, we show that dTAT is required for mechanically-induced activation of NOMPC, a microtubule-associated transient receptor potential channel, and functions to maintain integrity of the microtubule cytoskeleton in response to mechanical stimulation.
Professor Joshua Currie
Dept of Cell and Systems Biology