Multiple FGF pathway components modify Smn-dependent viability. (A) Schematic diagram depicting the FGF signaling pathway in Drosophila. In Drosophila, pathway activation is mediated by the two known FGF receptor orthologues, breathless (btl) and heartless (htl) (Glazer and Shilo, 1991). btl, which functions in the tracheal system, is activated by its ligand branchless (bnl) (Sutherland et al., 1996), whereas htl, which functions in the mesoderm and muscles, is activated either by the thisbe (ths) (Kerr et al., 2003) or pyramus (pyr) (Stathopoulos et al., 2004) ligands. Both receptors act through Sos-Grb2 to activate Ras/Raf/MAP kinase signaling. Additional regulation of Ras/Raf/MAP kinase signaling occurs through stumps (Vincent et al., 1998), which regulates the phosphatase corkscrew (csw) (Petit et al., 2004). In turn, Csw negatively regulates sprouty (sty), itself a negative regulator of Raf, thereby leading to MAPK activation (Jarvis et al., 2006). (B) The lethal phenotype associated with mesoderm-specific how24BGAL4-directed expression of UAS-Smn-RNAi^C24 is enhanced by the reduction of the FGF signaling pathway components htl, stumps, and breathless. (C) sprouty alleles suppress the how24BGAL4 UAS-Smn-RNAi lethal phenotype. Significant differences are indicated (*, P < 0.05; **, P < 0.01).