Optic Chiasm Presentation of Semaphorin6D in the Context of Plexin-A1 and Nr-CAM Promotes Retinal Axon Midline Crossing
Copyright policy )Optic Chiasm Presentation of Semaphorin6D in the Context of Plexin-A1 and Nr-CAM Promotes Retinal Axon Midline Crossing
At the optic chiasm, retinal ganglion cells (RGCs) project ipsi- or contralaterally to establish the circuitry for binocular vision. Ipsilateral guidance programs have been characterized, but contralateral guidance programs are not well understood. Here, we identify a tripartite molecular system for contralateral RGC projections: Semaphorin6D (Sema6D) and Nr-CAM are expressed on midline radial glia and Plexin-A1 on chiasm neurons, and Plexin-A1 and Nr-CAM are also expressed on contralateral RGCs. Sema6D is repulsive to contralateral RGCs, but Sema6D in combination with Nr-CAM and Plexin-A1 converts repulsion to growth promotion. Nr-CAM functions as a receptor for Sema6D. Sema6D, Plexin-A1, and Nr-CAM are all required for efficient RGC decussation at the optic chiasm. These findings suggest a mechanism by which a complex of Sema6D, Nr-CAM, and Plexin-A1 at the chiasm midline alters the sign of Sema6D and signals Nr-CAM/Plexin-A1 receptors on RGCs to implement the contralateral RGC projection.
- Icahn School of Medicine at Mount Sinai United States
- Osaka University Japan
- Howard Hughes Medical Institute United States
- Columbia University United States
- King’s University United States
Mice, Knockout, Retinal Ganglion Cells, Neuroscience(all), Nerve Tissue Proteins, Receptors, Cell Surface, Semaphorins, Axons, Retina, Mice, Optic Chiasm, Animals, Cell Adhesion Molecules, Cells, Cultured
Mice, Knockout, Retinal Ganglion Cells, Neuroscience(all), Nerve Tissue Proteins, Receptors, Cell Surface, Semaphorins, Axons, Retina, Mice, Optic Chiasm, Animals, Cell Adhesion Molecules, Cells, Cultured
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