Grant RoweIdentification of Amalgam and Neurotactin as Dominant Enhancers of the Abl Mutant Phenotype
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Axon outgrowth and directional pathfinding are processes that are vital to central nervous system (CNS) development. The Drosophila model system is useful to study highly conserved signaling pathways that lead to proper axon pathfinding. The gene for the Abelson tyrosine kinase (Abl) has been shown to be vital to such pathways. Many dosage-sensitive, genetic modifiers of the Abl mutant phenotype have been identified, thereby providing clues toward the mechanisms of the AblĀ-mediated signaling network and proteins involved in initiating and propagating signaling through Abl. Two genes that demonstrate novel genetic interactions with Abl encode the secreted adhesion molecule Amalgam (Ama) and its receptor Neurotactin (Nrt). In this study, mutational analyses of these loci have implicated this adhesion complex in the Abl network. Characterization of mutations in these proteins has provided insight into mechanisms of Ama-Nrt-mediated adhesion. We have also called into question the role of the disabled (dab) gene in neural development by proving that mutant alleles previously thought to be at this locus are actually at the nrt locus.

