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PMID:2406026
Citation |
Elkins, T, Zinn, K, McAllister, L, Hoffmann, FM and Goodman, CS (1990) Genetic analysis of a Drosophila neural cell adhesion molecule: interaction of fasciclin I and Abelson tyrosine kinase mutations. Cell 60:565-75 |
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Abstract |
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. |
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Keywords |
Alleles; Animals; Axons/physiology; Cell Adhesion Molecules, Neuronal/genetics; Chromosome Mapping; Drosophila/embryology; Drosophila/genetics; Morphogenesis; Mutation; Nervous System/embryology; Nucleic Acid Hybridization; Plasmids; Protein-Tyrosine Kinases/genetics; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins c-abl; Proto-Oncogenes; Transcription, Genetic |
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Significance
Annotations
Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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