(A) During late embryonic development, subsets of On DSGCs express the transmembrane protein Sema6A, arrive at the MTN target region and are attracted by cells in the MTN that express PlexA2 and PlexA4. PlexA2 and A4 serve as attractive ligands and signal through Sema6A to stabilize On DSGC-MTN innervation. Accurate connections between On DSGC axons and the MTN ensure correct assembly of AOS circuits critical for mediating the vertical OKR response. (B) In Sema6A−/− single mutants and PlexA2−/−;PlexA4−/− double mutants, On DSGC axons fail to correctly target the MTN and subsequently exhibit cell loss in the retina, thereby resulting in diminished vertical OKR responses. In addition, PlexA2−/−;PlexA4−/− double mutants show defects in RGC-DTN innervation, in line with the defective horizontal OKR responses observed in these double mutants (not shown).