Fig. 2. The glide complex affects muscle attachment. Anti-Myosin labelling reveals muscle organisation in early stage 17 embryos of the following genotypes: (A,C) wild type (WT); (B,D) glide-glide2 embryos (glide-glide2 lof); (E) glide embryos carrying one copy of glide2 (glide lof-glide2 +/lof); (F) glide-glide2 embryos specifically expressing glide in tendon cells (stripe-gal4 driver) (called Rescue); (G) ptc::glide^DN (glide^DN); and (H) ptc::glide^N7-4DN (glide^N7-4DN) embryos. (C,D) The regions delimited by dots in A,B, respectively. All panels show ventral views. Dashed line in C-H shows the ventral midline. In wild-type embryos (A,C), ventral longitudinal fibres attach to tendon cells at a distance from the midline. In glide-glide2 embryos (B,D), ventral longitudinal fibres bypass their target sites, attaching to others muscles at the midline (arrows in D). Note that muscle fibres normally attached to tendon cells that do not express glide are also indirectly affected. (E) Embryo carrying one copy of glide2 displays less severe phenotype than the double mutant. (F) The muscle phenotype is fully rescued by specifically expressing glide in tendon cells (n=10). (G) Inhibition of glide complex activity (ptc::glide^DN) induces the midline crossing phenotype (see arrow), whereas the inactive form of the dominant negative construct (ptc::glide^N7-4DN in H) does not. Scale bars: 50 µm.