bendless, a Drosophila gene affecting neuronal connectivity, encodes a ubiquitin-conjugating enzyme homolog.
The Drosophila bendless (ben) gene was originally isolated as a mutation affecting the escape jump response. This behavioral defect was ascribed to a single lesion affecting the connectivity between the giant fiber and the tergotrochanter motor neuron. A closer examination of the ben phenotype suggests that ben activity is broader and affects a variety of other neurons including photoreceptor cells and their axons. Mosaic analysis indicates that the focus of ben activity is presynaptic. We have cloned the ben gene through a chromosomal walk and show that it is homologous to a class of ubiquitin-conjugating enzymes. The major role of ubiquitination in the protein degradative pathway suggests that ben regulates neural developmental processes such as growth cone guidance by targeting specific proteins for degradation.
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Department of Entomology and Parasitology, University of California at Berkeley 94720.
McMahon
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Benzer
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Tanouye
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D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D002755:Choice Behavior / Q000502:physiology; D003001:Cloning, Molecular; D004330:Drosophila / Q000235:genetics*; D004924:Escape Reaction / Q000502:physiology*; D005121:Extremities; D007395:Interneurons / Q000502:physiology; D008969:Molecular Sequence Data; D009154:Mutation; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D017386:Sequence Homology, Amino Acid; D014452:Ubiquitins / Q000378:metabolism*; D014795:Visual Pathways / Q000502:physiology
D014452:Ubiquitins