Fig. 6. PLXNA3 and PLXNA4 cooperation during facial branchiomotor, but not visceromotor axon guidance.
(A-D) Wholemount neurofilament staining of wild type (A,C) and Plxna3/Plxna4 double null mutants (B,D) at 11.5 dpc reveals the vestibuloacoustic (VIIIg), facial (VIIg) and trigeminal ganglia (Vg) as well as the three main facial and trigeminal nerve branches. (A,B) A lateral view of the head in a wild type shows the three facial branches, the branchiomotor nerve (VIIbm), the chorda tympani (VIIct) and the greater superficial petrosal nerve (VIIgspn), as well the mandibular (Vmd), maxillary (Vmx), and ophthalmic (Vop) branches of the trigeminal nerve. (B) The combined loss of PLXNA3 and PLXNA4 disrupted the patterning of the facial branchiomotor nerve (white arrowhead) as well as the mandibular (black arrowhead), maxillary (black arrow) and ophthalmic (white arrow) trigeminal nerve branches more severely than loss of either plexin alone (compare B with Fig. 2H,I). (C) A ventral view shows that VIIgspn axons normally arborate in the area where the sphenopalatine ganglion forms (circled). (D) The combined loss of PLXNA3 and PLXNA4 caused defasciculation (arrows) and midline crossing (arrowheads) of VIIgspn axons, and there was no arborisation in the area where the sphenopalatine ganglion forms; however, defects were not worse than those caused by loss of PLXNA4 alone (compare D with Fig. 4I). Scale bar (A-D) 250 μm. (E) Working model for facial nerve patterning: SEMA3A and SEMA3F cooperate to pattern facial branchiomotor neuron (FBM) axons by binding to NRP1/PLXNA4 and NRP2/PLXNA3, respectively; SEMA3A also patterns facial visceromotor neuron (FVM) axons by binding to NRP1/PLXNA4 complexes.