Fig. 4. Disruption of optic stalk morphology in the Fak56D mutant. (A,B) R axons in a wild type (A) and a Fak56D^CG1 homozygous mutant (B), visualized with mAb24B10 (white). In a Fak56D mutant, R axons failed to be bundled (arrow). (C) Optic stalks in a wild type (0, left) and in Fak56D mutants (1-4), visualized with anti-Perlecan (white). Fak56D mutants exhibited defects in optic stalk morphology. Defects were classified into five groups (0-4), according to the severity of the phenotype. A dashed line indicates the eye disc-optic lobe boundary. Arrows indicate the optic stalk/optic lobe boundary. (D) Quantification of optic stalk defects in wild type and Fak56D mutants. The percentage of the brain that shows optic stalk defect is plotted as a function of severity level of the phenotype (0-4 in C). (E) Quantification of optic stalk defects in wild-type animals or Fak56D^CG1 homozygous animals at various developmental stages. Defects are not detected until the early third instar larval stage in Fak56D mutants, becoming progressively more severe during third instar larval stages. (F) Fak56D expression in the late third instar larvae. Brains and imaginal discs were stained with the Fak56D sense or the Fak56D antisense RNA probe. Fak56D is ubiquitously expressed. (A-C) Anterior up, dorsal right. AP, the height of the optic stalk; DV, the diameter of the optic stalk.