Homozygotes die at the end of embryonic development (stage 17) with a very thin cuticle in which the denticle belts are hardly visible. After removal of the vitelline membrane, the embryos can hardly move and die after a few minutes. There are no obvious patterning defects in the cuticle. The protein epicuticle layer is absent in mutant embryos and the thickness of the endocuticle is reduced. Microvilli can be seen at the surface of the epidermis in the mutant embryos. The distribution of the trachea is abnormal. Eggs derived from homozygous female germ-line clones have egg shells that show defects in dorsal-ventral patterning; the dorsal appendages are either separated by a smaller distance than normal, partially fused or completely fused. The distribution of egg shell phenotypes is similar in if the females are mated to either wild-type males or males carrying Sec61β¹⁴⁴⁴⁸. The embryos derived from homozygous female germ-line clones do not hatch, and die at a variety of developmental stages, with only a few reaching stages 16 or 17 at 25^oC. The stage of lethality varies with temperature; at 18^oC, 34.4% reach stages 16 and 17. The embryos have a very thin cuticle. The phenotype cannot be paternally rescued. Approximately 5% of ommatidia either lack photoreceptors or have morphological defects in homozygous clones in the eye. The number of rhabdomeres seen is often lower in apical sections than in more basal sections, suggesting defects in differentiation that cause the rhabdomeres not to form over the entire apical-basal extent of the retina. Photoreceptors are only rarely completely missing. Homozygous clones in the wing do not show any visible defects. Homozygous clones in the leg are associated with a severe reduction in size of the tarsal segments. This reduction in size often occurs distal to the clone.