Fig. 6. hs-ceh-2 is able to partially rescue the fly ems phenotype in the brain. Laser confocal images of stage 15 embryonic Drosophila brains, lateral views. Anterior is towards the left, dorsal is upwards. ceh-2 cDNA was expressed under the control of a heat-shock promoter at embryonic stage 11 in offspring of ems^9H83/TM3 sb Ubx-lacZ heterozygotes. Embryos were fixed at stage 15 and stained with anti-horseradish peroxidase (green) and anti-ß-galactosidase antibodies (not shown). Homozygous ems mutant embryos were recognized by the absence of anti-ß-galactosidase staining. (A) ems/+ heterozygous mutants have wild-type brain morphology. Head involution movements cause a backward bending of the brain towards the ventral nerve cord. Arrow in A indicates connectives at the level of neuromere b3. (B) ems/ems mutant embryos have no neurons or connectives between neuromere b1 and the ventral nerve cord (arrow) (Hirth et al., 1995). The frontal connectives that usually project to b3 (arrowhead in A) project ectopically into b1(arrowhead in B). (C) hs-ceh-2 is able to restore the missing neuromeres (arrow) and correct the projection of the frontal nerve (arrowhead) in homozygous ems mutants. Head involution movements do not occur in ems homozygous mutants (Jürgens et al., 1984) and are not restored by hs-ceh-2 expression (nor by hs-ems; data not shown). Therefore the angle between brain and ventral nerve cord is larger in rescued animals (C) compared with heterozygotes (A).