Fig. 1. schizo is required for commissure formation. Frontal views of dissected central nervous system (CNS) preparations of stage-16 embryos. (A-C) Stained for the presence of all CNS axons using Mab BP102. (D-F) Stained for the presence of the Myc epitope using Mab 9E10. (C) The midline glial cells are labeled by ß-galactosidase expression using the AA142 enhancer. Anterior is up. (A) Wild-type embryos are characterized by a regular arrangement of longitudinal connectives (lc) and segmental commissures (ac, pc). (B) In homozygous schizo^C1-28 mutant embryos the formation of commissures is reduced (arrow). The longitudinal connectives are thinner. (C) Homozygous schizo^U112 embryos display a stronger commissural phenotype. Most frequently the anterior commissure is affected (arrow). In neuromeres with reduced commissures the midline glial cells migrate toward the connectives (arrowhead). (D) In wild-type embryos the sema-myc marker is expressed in only a few neurons in each hemineuromer. The corresponding axons cross the midline in one fascicle and turn anterior within the longitudinal connective. (E,F) In mutant schizo^U112/C1-28 embryos the sema-myc marker cannot be detected in about 50% of the commissures. Within the longitudinal connectives we noted a defasciculation of the Myc positive axon bundles (arrow).