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Published February 23, 1990 | public
Journal Article

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 IONS 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 (abo 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 1 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 1 positive) does not follow its normal path across the commissure.

Additional Information

© 1990 Published by Elsevier Inc. Received September 29, 1989; revised December 20, 1989. We are indebted to D. Ferres-Marco for excellent technical support in mutant isolation and immunohistology. We also thank A. Kolodkin for supplying the P element mutation slit^(E158) , A. Bieber and N. Patel for the MAb BP102, R. Bennett, L. Y. Jan, and Y. N. Jan for supplying antibodies, and M. Seeger for comments on the manuscript. This work was supported by a Damon Runyon-Walter Winchell Cancer Postdoctoral Fellowship and Howard Hughes Medical Institute postdoctoral support to T. E., a Helen Hay Whitney Postdoctoral Fellowship to K. Z., a National Institutes of Health MSTP Traineeship to L. M., NIH grant CA49582 to F. M. H., and the Howard Hughes Medical Institute and NIH grant HD21294 to C. S. G. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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