ArticleGenes & genomics2026
The control of Plexin A-mediated axon guidance by the Src family kinase Src64B in Drosophila.
Article in Genes & genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe repulsive guidance function of PlexA was shown to require the intact intracellular region of PlexA protein, but not its RasGAP activity. Little is known about the molecular mechanisms by which activated PlexA receptors transmit guidance signals to steer growth cones.
objectiveTo examine whether Src family kinases (SFKs) are necessary for motor axon pathfinding in Drosophila, and how SFKs are involved in the regulation of PlexA-mediated axon guidance.
methodsLate-stage 16 embryos were fixed, permeabilized, and immunostained with anti-Fasciclin II (1D4) antibody to visualize the axonal projection pattern of motor neurons. Transfection of S2 cells, immunoprecipitation, and immunoblot analysis were conducted to quantify phosphorylation levels of PlexA proteins. We engineered a series of PlexA mutant constructs containing specific tyrosine-to-phenylalanine substitutions and generated transgenic flies for these mutant constructs. Using these PlexA mutant transgenes, genetic complementation and genetic interaction experiments between SFKs and PlexA derivatives in a gain-of-function paradigm were performed.
resultsGenetic analysis suggests that SFK Src64B is required for selective defasciculation of ISNb axons at specific choice points and target recognition. In cultured cells, Src64B downregulates the protein stability of PlexA through tyrosine phosphorylation. Moreover, genetic complementation using 9 PlexA mutant transgenes that contain substitution of single or double tyrosine residues to phenylalanines in their intracellular region demonstrates that multiple tyrosine residues are required for normal PlexA guidance functions. Finally, we found that coexpression of wild-type PlexA suppressed total ISNb motor axon defects induced by Src64B overexpression, whereas they were not suppressed but instead enhanced by coexpression of each of all tyrosine-to-phenylalanine mutant PlexAs.
conclusionTaken together, we propose that Src64B-mediated phosphorylation of PlexA negatively regulates PlexA signaling activity.
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