The Drosophila SHC adaptor protein is required for signaling by a subset of receptor tyrosine kinases

Receptor tyrosine kinases (RTKs) transduce signals via cytoplasmic adaptor proteins to downstream signaling components. We have identified loss-of-fun ction mutations in dshc, the Drosophila homolog of the mammalian adaptor pr otein SHC. A point mutation in the phosphotyrosine binding (PTB) domain com pletely abolishes DSHC function and provides in vivo evidence for the funct ion of PTB domains. Unlike other adaptor proteins, DSHC is involved in sign aling by only a subset of RTKs: dshc mutants show defects in Torso and DER but not Sevenless signaling, which is confirmed by epistasis experiments. W e show by double-mutant analysis that the adaptors DOS, DRK, and DSHC act i n parallel to transduce the Torso signal. Our results suggest that DSHC con fers specificity to receptor signaling.