iPLA2-VIA^EY05103 mutant adults show impaired locomotor behavior, as shown by a progressive and significant decrease in climbing capacity and a significantly decreased performance in the "equilibrist test", as compared to controls. These adults do not display olfactory associative learning and memory defects (in 2 days- and 2 weeks-old adults), as compared to controls. These adults show a progressive accumulation of apoptotic cells in the brain, as compared to controls.

iPLA2-VIA^EY05103 homozygous adult males exhibit progressive locomotor defects compared to controls: in open field assays 4 weeks old adults, but not 2 weeks old adults, show significant decreases in total walking distance, walking speed and proportion of active period; in equilibrist tests (individuals with clipped wings walking along a fine line) 2 weeks old adults show a significant decrease in walking distance, whereas 4 week old individuals are almost completely inactive and spend a considerable time balancing.

The iPLA2-VIA^EY05103 allele does not produce any gross changes in body size or obvious morphological defects compared with wild-type.

Homozygous iPLA2-VIA^EY05103 flies display progressive locomotor deficits, with the climbing ability of the mutants in response to light tapping progressively falling below that of wild-type from around 20 days of age. The mutant flies also show an approximately 50% reduction in lifespan, in both females and males.

Deuterated linoleic acid partially rescues the locomotor abnormalities but not the lifespan-defects of flies homozygous for iPLA2-VIA^EY05103.

The number of eggs laid per female by iPLA2-VIA^EY05103 mutants significantly declines with age compared with age-matched control flies, and by 25 days of age, the mutant flies are almost completely infertile.

Light microscopic examination of thin paraffin sections of homozygous iPLA2-VIA^EY05103 fly brains reveals normal brain architecture in young 2-day old flies that is indistinguishable from wild-type. However, by 32 days of age there is significant widespread vacuolation in the mutant brains that is not present in control brains. Ultrastructural examination using electron microscopy reveals that the mitochondria are grossly abnormal and swollen with fragmented cristae in 32-day old homozygous iPLA2-VIA^EY05103 mutant brains as compared with the mitochondria of age-matched wild-type brains or younger 2-day old iPLA2-VIA^EY05103-mutant brains, which are both filled with densely packed cristae. Furthermore, examination of the fly eye using electron microscopy reveals abnormal retinal structures in the 32-day old mutants compared with age-matched controls, with grossly abnormal ommatidial structure.

A significant reduction in mitochondrial membrane potential is revealed in homozygous iPLA2-VIA^EY05103 mutant fly brains compared with controls. Decreased oxygen consumption in state 3 respiration is also observed in comparison with wild-type. This defect worsens with age, as older flies have lower respiratory control ratio values.

Homozygous iPLA2-VIA^EY05103 flies show an age-dependent, progressive sensitivity to oxidative stress (exposure to hydrogen peroxide and paraquat), that is not consistently present in younger flies. Both younger and older flies are also sensitive to osmotic stress and show reduced survival compared with wild-type flies when fed 500 mM NaCl. The mutant flies also display increased sensitivity to hypoxic and xenobiotic (dichlorodiphenyltrichloroethane, DDT) stresses.

7-day old homozygous iPLA2-VIA^EY05103 flies are not sensitive to starvation, but become sensitive at day 15 of age compared with wild-type.