Abstract
Activation of the receptor tyrosine kinase (RTK) torso defines the spatial domains of expression of the transcription factors tailless and huckebein. Previous analyses have demonstrated that Rasl (p21ras) operates upstream of the D-Raf (Raft) serine/threonine kinase in this signaling pathway. By using a recently developed technique of germline mosaics, we find that D-Raf can be activated by torso in the complete absence of Rasl. This result is supported by analysis of D-Raf activation in the absence of either the exchange factor Son of sevenless (Sos) orthe adaptor protein drk (Grb2), as well as by the phenotype of a D-Raf mutation that abolishes binding of Rasl to D-Raf. Our study provides in vivo evidence that Raf can be activated by an RTK in a Ras-independent pathway.
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