Abstract
The five vestibular organs of the inner ear derive from patches of prosensory cells that express the transcription factor SOX2 and the Notch ligand JAG1. Previous work suggests that JAG1-mediated Notch signaling is both necessary and sufficient for prosensory formation and that the separation of developing prosensory patches is regulated by LMX1a, which antagonizes Notch signaling. We used an inner ear-specific deletion of the Rbpjκ gene in which Notch signaling is progressively lost from the inner ear to show that Notch signaling, is continuously required for the maintenance of prosensory fate. Loss of Notch signaling in prosensory patches causes them to shrink and ultimately disappear. We show this loss of prosensory fate is not due to cell death, but rather to the conversion of prosensory tissue into non-sensory tissue that expresses LMX1a. Notch signaling is therefore likely to stabilize, rather than induce prosensory fate.