Fig. 1. Genetic interactions in the CNS. (A-F) Preparations of stage 14 ventral nerve cords stained with mAb BP102. Anterior is upwards. (G,H) Stage 15 embryos stained with mAb 1D4 (anti-Fasciclin 2). (A) Wild-type CNS axon scaffold with anterior and posterior commissures (AC and PC) separating longitudinal connectives (LC). (B) Collapsed axon phenotype of a sim^H9 homozygote. (C) ‘Stalled axon’ phenotype of jing⁰¹⁰⁹⁴; sim^H9 double heterozygote. Arrow and arrowhead indicate improper commissural and longitudinal formation, respectively. (D) The axon scaffold develops properly in embryos heterozygous for sim^H9 and a jing⁰¹⁰⁹⁴ P element revertant (jing^rev). (E) The phenotype of embryos heterozygous for tgo¹ and jing⁰¹⁰⁹⁴ resembles weak sim phenotypes (arrow) and spitz group phenotypes (arrowhead). (F) Severe ‘collapsed axon’ phenotype in jing⁰¹⁰⁹⁴, tgo¹ sim^H9 triple heterozygote. (G) Three wild-type 1D4-positive longitudinal fascicles run parallel to the midline. (H) Fusion of longitudinal fascicles in jing⁰¹⁰⁹⁴, tgo¹ sim^H9 triple heterozygotes. (I) Quantification of jing genetic interactions. Double and triple heterozygotes (genotype) were examined for CNS axon scaffold formation using mAb BP102. Data are presented as the percentage of embryos with stalled, collapsed and fused axon phenotypes (n>50 embryos scored in all cases). Note that reduction of one copy of tgo in a jing⁰¹⁰⁹⁴; sim double heterozygote causes a shift in distribution from embryos with stalled axon phenotypes toward those with collapsed axon phenotypes (jing⁰¹⁰⁹⁴, tgo¹ sim^H9). jing⁰¹⁰⁹⁴ and sim^H9 mutations show similar dose sensitivities to sli¹.