From day 7, mp^f07253 flight performance gets significantly lower compared to controls. Mutants' indirect flight muscles exhibit frail appearance, especially at the epidermal-muscular junction; ultrastructurally, mitochondria show disorganized cristae with fuzzy outer membranes and vacuoles in the matrix, and quite a few mitochondria adjacent to myofilaments exhibit swollen appearance or blebbed outer membranes.

Cardiomyocytes of mp^f07253 mutants are filled with fewer myofilaments than controls, exhibit fragmented mitochondria embedded in an amorphous material, and have a broadened basement membrane at the luminal surface.

mp^f07253 adult thoraces show a significant decrease in ATP levels and an increase in reactive oxygen species.

mp^f07253 muscle degeneration is delayed by treatment with cyclosporin A; mitochondrial morphology is improved by treatment with losartan; and flight capability is improved with either drug.

The neurons of chordotonal organs have a blunt morphology in homozygous embryos.

Homozygous larvae show a poor response to physical stimuli (in contrast to wild-type larvae which show a strong avoidance response). Fatbodies are smaller than normal and their lipid droplets are large and sparse in homozygous larvae (in contrast to wild type where they are small and dense). Intercellular spaces between cells of the fat body are broader in homozygous larvae compared to wild type.

36.8% of homozygotes and 33.8% of mp^f07253/mp^f03008 adults show defects at the wing margin, where the longitudinal veins do not extend fully to the edge of the wing.

12.2% of homozygotes and 29.4% of mp^f07253/mp^f03008 adults show abnormalities in the dorsal abdominal cuticle (the tergites are either missing or not fused at the dorsal midline).

Cul3^EY11031, Mp^f07253 has abnormal neurophysiology | larval stage phenotype

Mp^f07253, inc^kk3 has abnormal neurophysiology | larval stage phenotype