Supporting cells in the cochlea change their shape in response to purinergic receptor activation, which influences hair cell excitability by altering potassium redistribution in the extracellular space.
Emx2 mediates the directional selectivity of neuromasts by regulating hair bundle orientation in hair cells, and by selecting afferent neuronal targets.
Hair follicle epithelium and skin vasculature remodeling are coordinated during quiescence, and their cross-talking is associated with the timing of stem cell activation.
Opposing gradients of activin A and follistatin within the spiral shaped mammalian cochlea instruct the graded pattern of mechano-sensory hair cell formation.
Other than its function in mechanotransduction, TMC1 is indispensable for action potential firing of auditory hair cells by mediating a leak conductance that alters tonotopically along the cochlea coil.
Direct reprogramming of somatic cells to an inner ear sensory hair cell-like state provides an experimental platform to identify causes and treatments for hair cell loss and hearing deficits.
The mammalian utricle can better regenerate hair cells compared to the cochlea because it maintains hair cell gene loci in a more transcriptionally accessible state.
Cell fate-mapping with genetically-modified mouse models and cellular markers demonstrates that sensory hair cells in the vestibular portion of the inner ear are a dynamic population in adult mice that undergo cell death and replacement under normal conditions.
