Abstract
Netrin-1 promotes outgrowth of axons in vitro through the receptor Deleted in Colorectal Cancer (DCC) and elicits turning of axons within embryonic explants when presented as a point source. It is not known whether netrin-1 alone can elicit turning nor whether DCC mediates the turning response. We show that Xenopus retinal ganglion cell growth cones orient rapidly toward a pipette ejecting netrin-1, an effect blocked by antibodies to DCC. In vitro, netrin-1 induces a complex growth cone morphology reminiscent of that at the optic nerve head, a site of netrin-1 expression in vivo. These results demonstrate that netrin-1 can function alone to induce turning, implicate DCC in this response, and support the idea that netrin-1 contributes to steering axons out of the retina.
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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Amino Acid Sequence
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Animals
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Antibodies / pharmacology
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Cell Adhesion Molecules / physiology*
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Cell Polarity
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DCC Receptor
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Embryo, Nonmammalian / physiology*
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Gene Expression Regulation, Developmental
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Humans
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Molecular Sequence Data
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Nerve Growth Factors / biosynthesis
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Nerve Growth Factors / pharmacology*
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Nerve Growth Factors / physiology*
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Netrin Receptors
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Netrin-1
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Neurites / drug effects
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Neurites / physiology
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Neurites / ultrastructure
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Optic Nerve / embryology
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Organ Culture Techniques
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Polymerase Chain Reaction
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Receptors, Cell Surface / immunology
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Receptors, Cell Surface / physiology*
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Retina / embryology*
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Retinal Ganglion Cells / cytology
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Retinal Ganglion Cells / drug effects
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Retinal Ganglion Cells / physiology*
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Sequence Alignment
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Sequence Homology, Amino Acid
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Transcription, Genetic
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Tumor Suppressor Proteins*
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Xenopus
Substances
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Antibodies
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Cell Adhesion Molecules
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DCC Receptor
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DCC protein, human
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NTN1 protein, human
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Nerve Growth Factors
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Netrin Receptors
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Receptors, Cell Surface
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Tumor Suppressor Proteins
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Netrin-1