Ratios of redox molecules are significantly shifted towards the oxidised form in homozygous and Tpisgk-1/Tpisgk-js10 animals compared to controls. This phenotype is age-dependent. Mitochondria in homozygous flies are oxidatively stressed, even at a young age.
Homozygous flies show a "bang sensitive" phenotype and show paralysis at high temperature. Both phenotypes are significantly worsened by treatment with hydrogen peroxide and is significantly improved by treatment with sub-lethal levels of beta-mercaptoethanol.
Homozygous flies are hypersensitive to hydrogen-peroxide mediated oxidative stress and resistant to high doses of beta-mercaptoethanol compared to controls.
The mechanical stress sensitivity of mutant animals is significantly improved if the animals are treated with MG132 or Geldanamycin.
Mutants show a bang sensitive phenotype at both room temperature and at 29[o]C, taking longer to recover from mechanical stress than control flies.
Tpisgk-1/Tpisgk-js10 flies take longer to regain normal locomotion after mechanical stress than control flies. This stress sensitivity is progressive and increases significantly with the age of the flies at all temperatures examined (room temperature, 25oC and 29oC). Severe stress sensitivity is evident much earlier in flies maintained at 25oC or 29oC compared to those raised at room temperature.
Lifespan of homozygous and Tpisgk-1/Tpisgk-js10 animals is significantly reduced compared to controls at room temperature, 25oC and 29oC. The decrease in lifespan compared to controls becomes more severe as the temperature at which the flies are raised is increased.
Young Tpisgk-1/Tpisgk-js10 adults do not show neuropathological defects, however, by their median age, they develop marked neuropathology, showing degeneration in the brain and thoracic ganglion. This degeneration is seen in flies raised at room temperature, 25oC and 29oC.
Mitochondria in the brain and the indirect flight muscle appear normal in homozygous adults.