Genetic analysis of a Drosophila neural cell adhesion molecule: interaction of fasciclin I and Abelson tyrosine kinase mutations.
Drosophila fasciclin I is a homophilic cell adhesion molecule expressed in the developing embryo on the surface of a subset of fasciculating CNS axons, all PNS axons, and some nonneuronal cells. We have identified protein-null mutations in the fasciclin I (fas I) gene, and show that these mutants are viable and do not display gross defects in nervous system morphogenesis. The Drosophila Abelson (abl) proto-oncogene homolog encodes a cytoplasmic tyrosine kinase that is expressed during embryogenesis primarily in developing CNS axons; abl mutants show no gross defects in CNS morphogenesis. However, embryos doubly mutant for fas I and abl display major defects in CNS axon pathways, particularly in the commissural tracts where expression of these two proteins normally overlaps. The double mutant shows a clear defect in growth cone guidance; for example, the RP1 growth cone (normally fas I positive) does not follow its normal path across the commissure.
Howard Hughes Medical Institute, University of California, Berkeley 94720.
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Elkins
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Zinn
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McAllister
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Hoffmann
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Goodman
D000483:Alleles; D000818:Animals; D001369:Axons / Q000502:physiology; D015816:Cell Adhesion Molecules, Neuronal / Q000235:genetics*; D002874:Chromosome Mapping; D004330:Drosophila / Q000196:embryology / Q000235:genetics*; D009024:Morphogenesis; D009154:Mutation; D009420:Nervous System / Q000196:embryology; D009693:Nucleic Acid Hybridization; D010957:Plasmids; D011505:Protein-Tyrosine Kinases / Q000235:genetics*; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016315:Proto-Oncogene Proteins c-abl; D011519:Proto-Oncogenes; D014158:Transcription, Genetic
D015816:Cell Adhesion Molecules, Neuronal; D011518:Proto-Oncogene Proteins; C051641:fasciclin I; D011505:Protein-Tyrosine Kinases; D016315:Proto-Oncogene Proteins c-abl