Abstract
Neuropilin-1 (NP-1) has been identified as a necessary component of a semaphorin D (SemD) receptor that repulses dorsal root ganglion (DRG) axons during development. SemA and SemE are related to SemD and bind to NP-1, but do not repulse DRG axons. By expressing NP-1 in retinal neurons and NP-2 in DRG neurons, we demonstrate that neuropilins are sufficient to determine the functional specificity of semaphorin responsiveness. SemA and SemE block SemD binding to NP-1 and abolish SemD repulsion in axons expressing NP-1. SemA and SemE seem to have a newly discovered protein antagonist capacity at NP-1 receptors, whereas they act as agonists at receptors containing NP-2.
Publication types
- Research Support, Non-U.S. Gov't
- Research Support, U.S. Gov't, P.H.S.
MeSH terms
- Animals
- Carrier Proteins / pharmacology
- Carrier Proteins / physiology*
- Cell Line
- Chick Embryo / cytology
- Ganglia, Spinal / drug effects
- Ganglia, Spinal / metabolism
- Glycoproteins / antagonists & inhibitors
- Glycoproteins / pharmacology
- Growth Cones / drug effects
- Humans
- Mice
- Nerve Growth Factors / pharmacology
- Nerve Growth Factors / physiology*
- Nerve Tissue Proteins / agonists*
- Nerve Tissue Proteins / antagonists & inhibitors*
- Nerve Tissue Proteins / pharmacology
- Nerve Tissue Proteins / physiology*
- Neuropilin-1
- Retinal Ganglion Cells / drug effects
- Semaphorin-3A
Substances
- Carrier Proteins
- Glycoproteins
- Nerve Growth Factors
- Nerve Tissue Proteins
- SEMA3A protein, human
- Sema3a protein, mouse
- Semaphorin-3A
- semaphorin A(V)
- Neuropilin-1