The maternally expressed Drosophila gene torso (tor) is a receptor tyrosine kinase that, when activated, initiates a signal transduction cascade that is responsible for the proper differentiation of the terminal, nonsegmented regions of the embryo. l(1)pole hole, the Drosophila raf-1 serine-threonine kinase homolog, and corkscrew, a tyrosine phosphatase, have been shown previously to function in this signal transduction pathway. We have identified other products in this pathway by carrying out a mutagenesis screen for dominant suppressors of a tor gain-of-function allele. More than 40 mutations, some of which fall into seven complementation groups, have been characterized genetically. Two of these correspond to mutations in ras-1 and Son of sevenless (Sos), which also function in the sevenless and EGF receptor (Der) tyrosine kinase pathways. The phenotypes of several other Su(tor) mutations suggest that they also function in other receptor tyrosine kinase-activated pathways at different times during Drosophila development.