Fig. 9
From: A molecular basis for water motion detection by the mechanosensory lateral line of zebrafish
Hypothetical roles of Tmc2b and Tmc2a in neuromast hair cells. a In wild-type fish, for one type of L1 neuromast variant, anterior-facing hair bundles depend completely on Tmc2b, but the posterior-facing hair cells depend on Tmc2b and a limited quantity of Tmc2a. In tmc2b −/− mutants, hair cells that take up fluorophore predominantly face posteriorly and contribute to microphonic potentials. Asymmetric uptake and microphonic potentials may be due to limited Tmc2a compensation, which permits the decreased passage of fluorophore and the diminished entry of small cations because fewer functional channels assemble. Those that do form have pores with decreased capacity for 4-Di-2-ASP entry. L1 hair cells do not function if they lack both Tmc2b and Tmc2a. b In wild-type fish, in this hypothetical model, each mechanotransduction apparatus of IO4 hair cells has a similar molecular composition irrespective of hair bundle orientation, influenced by high levels of both Tmc2b and Tmc2a. In tmc2b −/− knockout fish, Tmc2a compensates for Tmc2b, resulting in a modest change in channel pore quality. IO4 hair cells do not function if they lack both Tmc2b and Tmc2a. Note, these models do not distinguish between Tmc2a and Tmc2b as accessory proteins of the mechanotransduction apparatus or as pore loop-containing channel subunits. They do however explain how mechanotransduction may be impacted by Tmc2a and Tmc2b
