Figure 6.

Working models of HC regeneration. A, In undamaged neuromasts, local signaling between mature HCs and internal SCs keeps cells quiescent. This process is not Notch dependent, and the inhibitory signal from the mature HCs is still unknown. After neomycin-induced death, internal SCs (IS) divide and give rise to two postmitotic HC precursors (HP). These HC precursors then differentiate into two new HCs. A second signal from the HC precursors signals to the adjacent internal SCs to inhibit proliferation and limit HC production. This second inhibitory signal is via Delta-Notch, which regulates and limits the number of regenerated HCs. B, When Notch signaling is inhibited with DAPT during regeneration, an increased number of internal SCs enter the cell cycle caused by no inhibition, resulting in an overproduction of HCs.