Semaphorin Signaling Neuron Hung-Hsiang Yu, Alex L Kolodkin  Neuron  Volume 22, Issue 1, Pages 11-14 (January 1999) DOI: 10.1016/S0896-6273(00)80672-8

Figure 1 Semaphorins and Their Receptors A schematic representation of semaphorin receptor/ligand interactions (arrows) identified thus far. The eight known semaphorin classes are shown (1–7 plus “V” [viral semaphorins]), as are the two known plexin classes and the neuropilins. All vertebrate plexins except VESPR have the same overall structure as that depicted for Drosophila Plexin A. Amino-terminal labels denote specific proteins discussed in text, and color coding denotes structural motifs. The structural motifs in the extracellular domains of neuropilins are not related in any way to the extracellular domains of plexins. Ig, immunoglobulin; GPI, glycosylphosphatidylinositol-linked; MRS, Met-related sequences; G-P, glycine proline repeats. Neuron 1999 22, 11-14DOI: (10.1016/S0896-6273(00)80672-8)

Figure 2 PlexA and Sema1a Exhibit Genetic Interactions Indicative of a Receptor/Ligand Pair Required for Repulsive Motor Axon Guidance Schematics of Drosophila embryonic motor axon branches in the ventral muscles of abdominal segments in wild-type and in various genetic backgrounds are shown with both internal lateral (left) and cross sectional (right) views of a subset of muscles and motor axon pathways. (A) Wild-type, Sema1a/+, and PlexA/+ embryos display a normal ISNb pathway. ISNb phenotypes in PlexA/PlexA embryos (see [B]) are partially suppressed in FasII/+;PlexA/PlexA embryos. (B) In the indicated genetic backgrounds, the ISNb shows defasiculation defects (see text). (C) In wild-type embryos that ectopically express Sema 1a on muscles 6 and 7 (orange), RP3 fails to defasciculate from the ISNb and form its normal synaptic arborization. (D) This RP3 defasiculation phenotype (shown in [C]) can be partially suppressed by removal of one copy of PlexA. Neuron 1999 22, 11-14DOI: (10.1016/S0896-6273(00)80672-8)