At the ultrastructural level, homozygous embryos show a separation of the apical extracellular matrix (cuticle) from the apical surface of the epidermis. All elements of the external epicuticle appear to be properly formed and remain in tight contact with the upper layers of the endocuticle. However, the chitin layer of the endocuticle has disintegrated, especially towards its basal side. An electron dense layer, presumably corresponding to a defective deposition zone, is faint and discontinuous compared to the wild-type deposition zone, and its typical tight contact to the chitin layer above is lost. On the apical surface of the mutant epidermal cells, the typical microvilli can still be seen, often attached to the remaining fragments of the deposition zone. Junctional structures within the mutant epidermal cells appear normal. The apical and basal junctions of tendon cells are intracellularly connected by large microtubule bundles in the mutant embryos and at the apical side, long tonofilaments extend away into the extracellular space (as occurs in wild type). Normally, tonofilaments anchor in the cuticle, however, in the mutant embryos, they appear to have been pulled out. The basal adhesive junctions of the tendon cells appear normal in the mutant embryos and the attachment of the basal surface of the rest of the epidermal cells to the basement membrane also appears normal.
Homozygous clones in the wing produce wing blisters. Blisters are associated with both dorsal and ventral clones. The pattern of veins and trichome polarity is normal, and there is no overgrowth or disruption to the overall wing shape and pattern.
Selected as: Mutation that produces wing blister in homozygous clones.