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Statoacoustic ganglion (SAG) neurons project sensory afferents to appropriate targets in the inner ear to form functional vestibular and auditory circuits. Neuropilin1 (Npn1), a receptor for class 3 semaphorins, is required to generate appropriate afferent projections in SAG neurons; however, the ligands and coreceptors involved in Npn1 functioning remain unknown. Here we show that both  plexinA1  and  plexinA3  are expressed by SAG neurons, and  plexinA1/plexinA3  double mutant mice show defects in afferent projections of SAG neurons in the inner ear. In control mice, sensory afferents of SAG neurons terminate at the vestibular sensory patches, whereas in  plexinA1/plexinA3  double mutants, they extend more dorsally in the inner ear beyond normal vestibular target areas. Moreover, we find that  semaphorin3a  ( Sema3a)  is expressed in the dorsal otocyst, and  Sema3a  mutant mice show defects in afferent projections of SAG neurons similar to those observed in  plexinA1/plexinA3  double mutants and in mice lacking a functional Npn1 receptor. Taken together, these genetic findings demonstrate that Sema3a repellent signaling plays a role in the establishment of proper afferent projections in SAG neurons, and this signaling likely occurs through a receptor complex involving Npn1 and either plexinA1 or plexinA3.

Deletion of Sema3a or plexinA1/plexinA3 Causes Defects in Sensory Afferent Projections of Statoacoustic Ganglion Neurons