Fig. 2. Loss of Gliolectin perturbs commissure formation. BP102 staining of embryos from late stage 12 through late stage 13 (A,F, stage 12/1; B,G, stage early 13; C,H, stage mid 13; D,I, stage late 13; E,J, stage early 14) shows the progressive development of distinct, well separated commissures in wild type (OreR, A-E) and the effects of loss of Gliolectin in 3013 homozygotes (-/-, F-J). In OreR embryos at stage 12/1, commissural axons (A, arrowhead) are diffusely spread among the midline glia but by early stage 13 (B, arrowhead) commissural separation is becoming apparent. In 3013 homozygotes, however, the commissures are tightly fasciculated into a single bundle in late stage 12 and early stage 13 embryos (F,G, arrowhead) and remain poorly separated into mid-stage 13 (H, arrowhead). By mid-stage 13, wild-type commissures (C, arrowhead) have separated into anterior and posterior bundles and the longitudinal pathways (arrow) are evident within each segment. In 3013 homozygotes at mid-stage 13, the forming longitudinals possess less axon density than wild-type (compare arrows in C and H). Partial commissural fusions and distortions remain common in late-stage 13 and early-stage 14 deletion homozygotes (I,J, arrowheads). Scale bar: 11 µm.