Raf kinase domain, with a valine replacing the conserved lysine in the ATP binding site, fused to the signal sequence, intracellular and transmembrane domains carrying the amino acid replacement characteristic of the tor13D protein, expressed from the sev enhancer and a heat shock promoter.
Demonstrates that dominant eye phenotype of phl::tor13D.hs.sev is caused through the action of the phl kinase.