Fig. 6. Glial expression of transgenic Rac1 disrupts migration and nerve ensheathement. repo:GAL4 embryos carrying the UAS-actin-GFP marker were used as the wild type (A-C). The repo::actin-GFP flies were also crossed to lines carrying UAS-Rac1V12 (D-F), UAS-Rac1wt (G-I), UAS-Rac1L89 (J-L) and UAS-Rac1N17 (M-O). Embryos were stained with anti-GFP (green) and mAb 22C10 (red). (A,D,G,J,M) Green channels. (B,E,H,K,N) Red channels. (C,F,I,L,O) Merge. Anterior is towards the top, CNS is towards the left. Embryos are stage 16. (D) Rac1V12 embryos have collapsed glial sheaths (concave arrows) as well as migration defects (solid arrow). The lateral line glia fail to connect across hemisegments (compare arrowhead with those in A). (E) The underlying sensory axon tracts are defasciculated in Rac1V12 embryos (arrows). (G) Overexpression of wild type Rac1 causes abnormal glial wrapping which is often overgrown in appearance compared with wild type (concave arrow). The lateral line glia do not consistently connect across hemisegments (arrowhead). (J) The Rac1L89 embryos show ectopic lamellar-like projections (concave arrows) as well as failed inter-connection of lateral line glia (arrowhead). (K) The underlying sensory axonal tracts are defasciculate (solid arrow). Misplacements of sensory neurons in Rac1L89 mutants (concave arrows) appear to be associated with glia (compare concave arrows in upper hemisegment in J,K). (M) Rac1N17 embryos have mildly disrupted glial wrapping profiles with occasional small gaps in the nerve sheath (arrow). (N) Sensory neurons in Rac1N17 embryos show defasciculation (arrow).