Activation of the Drosophila C3G leads to cell fate changes and overproliferation during development, mediated by the RAS–MAPK pathway and RAP1

摘要: The cellular signal transduction pathways by which C3G, a RAS family guanine nucleotide exchange factor, mediates v‐ crk transformation are not well understood. Here we report the identification of Drosophila which, like its human cognate, specifically binds to CRK but DRK/GRB2 adaptor molecules. During development, constitutive membrane binding also occurs during transformation, results in cell fate changes and overproliferation, mimicking overactivity RAS–MAPK pathway. effects C3G can be suppressed reducing gene dose components pathway RAP1. These findings provide first vivo evidence that localization trigger activation RAP1 resulting MAPK, one hallmarks previously thought mediated through SOS.