Fig. 7. jing mutations disrupt CNS midline glial differentiation. (A-D) Embryos stained with anti-SIM; (E,F) ß-gal expression in embryos carrying sli reporter P[sli 1.0 HV-lacZ]; (G,H) anti-SLI stain to visualize midline glia; (I-J') Stage 12 embryos double labeled with anti-SLI (green) and TUNEL (red), and confocal images of 1 µm serial sections. Sagittal views with anterior towards the left. (A,B) sim expression is reduced (arrow) in stage 9 jing³ homozygotes (B) compared with wild-type (A). (C,D) Reduced SIM immunoreactivity and small size of midline neurons (arrows) and glia (arrowheads) in stage 15 jing³ homozygotes (D) compared with wild-type (C). (E) Wild-type stage 11 expression of P[sli 1.0 HV-lacZ] in six midline glia. (F) P[sli 1.0 HV-lacZ] expression in average of 3.2 midline glia/segment in stage 11 jing³ homozygotes. (G) Wild-type SLI-positive glia during stage 15. (H) Reduced SLI immunoreactivity (arrowhead) and detection in macrophages outside the nerve cord (arrow) in stage 15 jing³ homozygotes. (I) Stage 12 wild-type sli-lacZ expression (green). TUNEL-positive profiles (red) are present only outside the CNS (arrow). (I') Close-up view of I. SLI- and TUNEL-positive glia (arrowhead). (J) Loss in SLI immunoreactivity (arrowheads) in stage 12 jing³ homozygotes. Note increase in TUNEL labeling compared with wild type. (J') Close-up view of J (arrows, dead glia). TUNEL-positive profiles in the nerve cord (arrowhead).