Fig. 6. jing loss- and gain-of-function phenotypes in the CNS and trachea. Frontal views showing CNS axon scaffolds (BP102 stain) (A-F) and longitudinal fascicles (mAb 1D4 stain; anti-Fasciclin 2) (G,H). Sagittal views of stage 15 whole-mount embryos stained with mAb 2A12 to visualize tracheal tubules (I-L). (A,B) Pioneering growth cones do not approach the midline during stage 12 in homozygous jing³ mutants (B) as they do in wild-type (A) (arrowheads). (C,D) In stage 14 jing³ mutants, there are variable absences of either anterior or posterior commissures (arrow) and longitudinal connectives (arrowhead) (D) compared with wild type (C). (E) jing³;sim^H9 double mutants show collapsed axon phenotypes. (F) Overexpression of jing in the CNS midline (sim-GAL4/jing-UAS) disrupts commissural (arrow) and longitudinal axon formation (arrowhead). (G) Ipsilateral projection of wild-type Fasciclin 2-positive longitudinal bundles. (H) In jing³ homozygotes, longitudinal fascicles inappropriately cross the midline (arrows). Longitudinal fascicles stall within segments (arrowhead). (I,J) Embryos homozygous for a deficiency covering jing (Df(2R)ST1) and jing³ mutations show defects in the formation of all tracheal branches, including the dorsal trunk (arrowhead) and transverse connectives (TC) (arrow). Note absence of the visceral branch (compare with Fig. 3A). (K) jing³; trh¹ double mutants show loss of all tracheal tubules. (L) Overexpression of jing in the trachea (btl-GAL4/jing-UAS) disrupts all aspects of tracheal tubule development. Branch fusion in the dorsal trunk does not occur (arrowhead) and the dorsal branch and transverse connectives are reduced (arrows). The visceral branch is absent. DB, Dorsal branch; VB, visceral branch; DT, dorsal trunk; TC, transverse connective; LTa, lateral trunk anterior; LTp, lateral trunk posterior.

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