A ROLE FOR ABL IN NOTCH SIGNALING

Abl is an axonal tyrosine kinase that has yet to be clearly linked to a receptor; Notch is a receptor for which the signaling pathway remain s incompletely understood. We show here that Notch and abl mutations i nteract synergistically to produce synthetic lethality and defects in axon extension. Surprisingly, we cannot account for these axonal aberr ations on the basis of changes in cell identity. We show, moreover, th at Notch is present in the growth cones of extending axons, and that t he Abl accessory protein Disabled binds to a signaling domain of Notch in vitro. We therefore speculate that Disabled and Abl may play a rol e in Notch signaling in Drosophila axons, perhaps by binding to the No tch intracellular domain.