The anterior and posterior commissures fail to separate correctly in homozygous embryos and the longitudinals are thinner than normal, and are collapsed towards the midline in places. Only a small number of neuromeres are affected in each embryo.

Loss of vein mutation. Suppression of rho^hs.PSt ectopic vein phenotype and enhancement of the rho^ve-1 loss of vein phenotype.

Mutant embryos show reduced width of denticle belts (reminiscent of mutations in the spitz group of genes). Denticle belts are disturbed particularly in the third thoracic segment and the regular spacing of the commissures and connectives of the CNS is perturbed. Filzkorpers have abnormal shape suggesting that their connection to the tracheal trunk has failed. Dorsal trunk and branches of the tracheal system are lacking. Instead the tracheal pits form abnormal cavities that remain disconnected. Clones in the wing are smaller than controls and affect the differentiation of wing structures. In proximal regions they cause fusion of vein trunks and both dorsal and ventral clones autonomously fail to differentiate veins. The effect is restricted to the surface in which the clone lies. Dorsal clones in veins LIII and LIV cause both loss of and thickened vein, often resulting in folding of the wing. Ventral clones in the posterior compartment close to vein LIV can cause vein loss. Veins in the anterior wing margin are not affected. Dorsal and ventral clones between veins LIII and LV produce ectopic bristles, with features of wing margin bristles.

vvl^Zm has larval ventral nerve cord commissure phenotype, enhanceable by D^r11

vvl^Zm has larval longitudinal connective phenotype, enhanceable by D^r11

vvl^Zm is an enhancer of larval ventral nerve cord commissure phenotype of D^r11

vvl^Zm is an enhancer of larval longitudinal connective phenotype of D^r11