Homozygous embryos do not show commissural defects. Many glec^m98/Df(3R)e-BS2 embryos have commissural defects at stage 12 to 13, with 78% of segments being affected. glec^m24/glec^m98 embryos show distortion, fusion and thinning of the commissures at stage 13 and a minimal loss of mass of the longitudinal connectives. The pCC axon does not extend as far anteriorly in glec^m98/Df(3R)e-BS2 embryos as in wild type at stage 12/1, and appears stalled after minimal outgrowth. Few pCC cells show extension beyond their segment of origin, even into late stage 13.