Mutation within the salm coding region, introduction of a stop codon.
wing & macrochaeta
Homozygous mutant, or salm16/salmFCK-25 clones in the antenna appear normal.
salmFCK-70/salm16 animals die as larvae.
Clone on the dorsal surface of the wing between wing vein L2 and L3 causes branching of the wing vein L2 on the presumptive dorsal surface; forked L2 phenotype. The ectopic vein forms within and at the extreme anterior edge of the clone. When the clone extends to the margin ectopic triple row bristles are formed. Clones near the posterior wing edge cause bifurcation of wing vein L5 or the posterior crossvein.
Lateral and ventral structures of the tracheal system are not affected. However the dorsal trunk is not properly assembled. Dorsal trunk cells migrate predominantly in a dorsal direction. Sporadic horizontal branches are formed but they occur at ectopic dorsal positions of tracheal metameres. Mutant embryos do not fail to specify the dorsal trunk homotip cells, and show no increased cell death. Mutants develop three ectopic tracheal placodes, Tr-1, Tr0 and Tr11, in addition to the ten wild type placodes. The sizes of Tr-1 and Tr11 are reduced with respect to wild type.
