Krn27/Krn9 enhances the wing vein phenotypes seen in vnL6/vn1 mutants. A greater proportion of flies show longitudinal vein 3 loss than in vnL6/vn1 alone. The phenotype is further enhanced by one copy of spi1.
Wings of homozygous pk30, rhove-1 and vn1 triple mutant flies lack veins L2-5. Wing anterior hairs of these mutants consistently have a posterior component to their polarity and posterior hairs have an anterior component to their polarity.
rhove-1 vn1 double homozygotes lack wing veins. This phenotype is partially suppressed by ash2S112411 /ash2S112411. The degree of suppression varies from development of L2 only to almost complete rescue, albeit with some abnormalities such as extra crossvein material or proximal fusions between L2 and L3 or L4 and L5. In 25% of cases, hollow, tube like wings are formed, probably due to detachment of dorsal and ventral layers.
The vn1/vnddd-3 loss of wing vein L4 phenotype is suppressed by emc1/emc11. emcD enhances the loss of wing veins seen in vn1/vnddd-3 flies. emc1 clones in rhove-1 vn1 wings differentiate as veins in positions possibly corresponding to those of wild-type veins. Vein differentiation in these clones frequently fails in distal regions of veins.
rhove-1 vn1 double mutant flies lack all the longitudinal veins and crossveins of the wing blade. Dorsal and ventral implants of rhove-1 vn1 imaginal disc tissue into wild-type imaginal discs fail to differentiate veins.