Mutants die as stage 17 embryos or during hatching and show no obvious defects in the formation of somatic and visceral muscles. At the end of embryogenesis embryos are severely paralysed, only twitching movements can be observed and their abdominal segments are strongly contracted. syt staining reveals the neuromuscular junctions can assemble normally. The extracellular tendon matrix (TM) is severely reduced, the muscles are forced to compete for epidermal surface at the segment border. At the ultrastructural level the thick and thin filaments are less ordered and dense in muscles, I-bands are absent, Z-bands are absent and instead only spindle-like concentrations of dark thin fibers can be seen.

Mutant clones in the eye exhibit phenotypic defects in many mutant ommatidia, the rhabdomeres of up to 4 outer photoreceptors have a smaller diameter resembling the rhabdomeres of receptor cell R7. All photoreceptors are abnormally differentiated and have malformed rhabdomeres that frequently do not extend into basal regions of the retina.