enabled, a dosage-sensitive suppressor of mutations in the Drosophila Abl tyrosine kinase, encodes an Abl substrate with SH3 domain-binding properties.

摘要: Genetic screens for dominant second-site mutations that suppress the lethality of Abl in Drosophila identified alleles only one gene, enabled (ena). We report ena protein contains proline-rich motifs and binds to Src SH3 domains, is also a substrate kinase; tyrosine phosphorylation increased when it coexpressed cells with human or endogenous reduced mutant animals. Like Abl, expressed at highest levels axons embryonic nervous system embryos have defects axonal architecture. conclude critical function phosphorylate negatively regulate during neural development.