Molecules antigenically similar to agrin, a protein extracted from the electric organ of Torpedo californica, are highly concentrated in the synaptic basal lamina of neuromuscular junctions in vertebrate skeletal muscle. On the basis of several lines of evidence it has been proposed that agrin-like molecules mediate the nerve-induced formation of acetylcholine receptor (AChR) and acetylcholinesterase (AChE) aggregates on the surface of muscle fibers at developing and regenerating neuromuscular junctions and that they help maintain these postsynaptic specializations in the adult. Here we show that anti-agrin monoclonal antibodies selectively stain the cell bodies of motor neurons in embryos and adults, and that the stain is concentrated in the Golgi apparatus. We also present evidence that motor neurons in both embryos and adults contain molecules that cause the formation of AChR and AChE aggregates on cultured myotubes and that these AChR/AChE-aggregating molecules are antigenically similar to agrin. These findings are consistent with the hypothesis that agrin-like molecules are synthesized by motor neurons, and are released from their axon terminals to become incorporated into the synaptic basal lamina where they direct the formation of synapses during development and regeneration.
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1 November 1988
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November 01 1988
Motor neurons contain agrin-like molecules.
C Magill-Solc,
C Magill-Solc
Stanford University School of Medicine, Department of Neurobiology, California 94305.
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U J McMahan
U J McMahan
Stanford University School of Medicine, Department of Neurobiology, California 94305.
Search for other works by this author on:
C Magill-Solc
Stanford University School of Medicine, Department of Neurobiology, California 94305.
U J McMahan
Stanford University School of Medicine, Department of Neurobiology, California 94305.
Online ISSN: 1540-8140
Print ISSN: 0021-9525
J Cell Biol (1988) 107 (5): 1825–1833.
Citation
C Magill-Solc, U J McMahan; Motor neurons contain agrin-like molecules.. J Cell Biol 1 November 1988; 107 (5): 1825–1833. doi: https://doi.org/10.1083/jcb.107.5.1825
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