Fig. 6. kette antagonizes scar/wave function. Frontal views of embryonic nerve cords of stage 16 embryos. Axon tracts are labeled using Mab BP102 and HRP immunohistochemistry (brown), midline glia cells are labeled in blue (enhancer trap insertion AA142). (A) In a wild-type nerve cord, two commissures are found in each neuromere (anterior commissure, ac; posterior commissure, pc). They are clearly separated by the midline glia (star). (B) In homozygous mutant kette^C3-20 embryos the segmental commissures are not separated into distinct axon bundles and instead appear fused. (C) Removal of one copy of the scar/wave gene in a homozygous mutant kette^C3-20 embryo significantly restores CNS development and commissures are recognizable as distinct axon bundles. (D) Homozygous mutant scar/wave embryos display no mutant CNS phenotype. (E) Reduction of wasp function in a kette mutant embryo (wasp kette double mutant) does not modify the mutant kette phenotype. (F) Expression of a membrane-tethered Kette protein can rescue the kette mutant phenotype. A rho-GAL/UAS-kette^Myr; kette^C3-20/kette^C3-20 embryo is shown. Scale bar: 30 µm.