OxTalks will soon move to the new Halo platform and will become 'Oxford Events.' There will be a need for an OxTalks freeze. This was previously planned for Friday 14th November – a new date will be shared as soon as it is available (full details will be available on the Staff Gateway).
In the meantime, the OxTalks site will remain active and events will continue to be published.
If staff have any questions about the Oxford Events launch, please contact halo@digital.ox.ac.uk
We have examined the role of transmembrane channel-like protein, TMC1, as the central component of the hair cell mechanotransducer (MET) channel by characterizing transduction in mice harboring mutations in the putative pore region, TM domains 4-7. Two mutations (Tmc1 p.D528N or Tmc1 p.E520Q) decreased channel conductance and two (Tmc1 p. D569N or Tmc1 p.W554L) lowered expression. All Tmc1 mutations reduced Ca2+ influx into the hair bundle. These mutations ultimately led to hair cell apoptosis and deafness by four weeks post-natal and corroborate TMC1 as the MET channel pore. The channel complex also contains the accessory subunit, LHFPL5. In Lhfpl5 knockout mice, MET currents could still be activated by hair bundle deflections but were reduced in amplitude and sensitivity. The working range and half-saturation of the MET current were increased and gating stiffness virtually abolished, suggesting LHFPL5 is part of the mechanical coupling between the tip-link PCDH15 and TMC1.
