Abstract
Semaphorins comprise a large family of phylogenetically conserved secreted and transmembrane glycoproteins, many of which have been implicated in repulsive axon guidance events. The transmembrane semaphorin Sema-1a in Drosophila is expressed on motor axons and is required for the generation of neuromuscular connectivity. Sema-1a can function as an axonal repellent and mediates motor axon defasciculation. Here, by manipulating the levels of Sema-1a and the cell adhesion molecules fasciclin II (Fas II) and connectin (Conn) on motor axons, we provide further evidence that Sema-1a mediates axonal defasciculation events by acting as an axonally localized repellent and that correct motor axon guidance results from a balance between attractive and repulsive guidance cues expressed on motor neurons.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Genetically Modified
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Axons / physiology*
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Cell Adhesion Molecules / genetics
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Cell Adhesion Molecules / physiology*
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Cell Adhesion Molecules, Neuronal / genetics
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Cell Adhesion Molecules, Neuronal / physiology*
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Connectin
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Crosses, Genetic
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Drosophila melanogaster / genetics
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Drosophila melanogaster / physiology*
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Fasciculation
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Female
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Genotype
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Glycoproteins / genetics
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Glycoproteins / physiology*
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Male
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Muscle Proteins / genetics
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Muscle Proteins / physiology*
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Nerve Growth Factors / genetics
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Nerve Growth Factors / physiology*
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Protein Kinases / genetics
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Protein Kinases / physiology*
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Semaphorin-3A
Substances
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Cell Adhesion Molecules
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Cell Adhesion Molecules, Neuronal
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Connectin
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Glycoproteins
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Muscle Proteins
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Nerve Growth Factors
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Semaphorin-3A
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fasciclin II
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Protein Kinases