Fig. 1.

Genetic interactions between kuz, slit, robo and comm. (A-L) Stage 16 embryos were stained with MAb BP102 (A-D,K,L) or MAb FasII (E-J) to reveal all CNS axons or subsets of ipsilateral axons, respectively. Anterior is up. (A) A wild-type embryo exhibiting the characteristic ladder-like axon scaffold. (B) A robo mutant embryo; note the reduction in thickness of the longitudinal connectives and the commensurate thickening of the commissures. (C) kuz mutants also show thinning of the longitudinals and thickening of the commissures. (D) In kuz mutants that are simultaneously heterozygous for slit and robo, the thickening of the commissures is qualitatively enhanced. (E) A wild-type embryo has three bundles of FasII-positive axons that do not cross the midline. (F) In robo mutant embryos, the medial bundle of FasII-positive axons wanders back and forth across the midline (arrowheads with asterisks). (G) kuz zygotic mutants have a milder crossing defect (arrows with asterisks), a phenotype that is enhanced when slit and robo are also heterozygous (H). (I) A slit, robo/+ embryo with a mild midline crossing defect (arrow with asterisk). (J) An example of a slit, robo/+, kuz/+ embryo showing dominant enhancement (arrows with asterisks). (K) comm mutant embryos completely lack axon commissures, whereas kuz; comm double mutants reveal a partial restoration of commissure formation (arrows in L).