Fig 2: Loss of sema-mediated activation of neuropilin-1 causes increased sensory domain innervation.(A-F) Whole mount samples from E16.5 cochleae from WT and Nrp1sema-/sema- mice. Neurons were stained with anti-TUJ1 antibodies (green) and hair cells were stained with anti-Myo6 antibodies (red). The arrows in D and F point to excessive nerve fibers innervating the hair cell region. Panels C and D show TUJ1 labeling with Sox2 immunolabeling, which identifies the different supporting cell types. OHC, outer hair cell; IHC, inner hair cell; dc, Deiters’ cell; opc, outer pillar cell; ipc, inner pillar cell. (G-N) Analysis of SGN afferents (Syt1 staining; magenta) and olivocochlear efferents (Gap43 staining; green) from E18.5 cochleae from WT and Nrp1sema-/sema- mice. The arrows in panels M and N point to an aberrant nerve fiber in the OHC region of Nrp1sema-/sema- cochleae. The arrowheads in M and N point to a cluster of nerve fibers that appears to be traversing across the cochlear radial fibers in an unusual manner. (O) Panel O showing that loss of Sema-mediated activation of neuropilin-1 can lead to a significant increase in Syt+ SGN processes projecting into the OHC region.