Flies expressing DysdsRNA.N.Scer\UAS under the control of either Scer\GAL4tub.PU or Scer\GAL4how-24B show significantly impaired recovery after being challenged by acute severe hypoxia exposure.
Flies expressing DysdsRNA.N.Scer\UAS under the control of Scer\GAL4tub.PU have a significantly impaired climbing index compared to wild type.
Flies expressing DysdsRNA.N.Scer\UAS under the control of either Scer\GAL4tub or the muscle-specific driver Scer\GAL4how-24B, show comparable climbing ability at the beginning of adult life to control flies. However, the ability of these animals to climb declines significantly faster over time compared to controls. By 12 days (when expression is driven by Scer\GAL4tub) or 20 days (when expression is driven by Scer\GAL4how-24B), age-dependent muscle degeneration is observed including loss of muscle fibre organisation, vacuolisation and the absence of some muscles.
Expression of DysdsRNA.N.Scer\UAS in the eye disc (under the control of Scer\GAL4GMR.PU), or in all glial cells (under the control of Scer\GAL4repo.PU), both result in photoreceptor axon targeting defects. Axons stop irregularly, making gaps in the normal termination zone of the lamina plexus, deviating from the path and bundling aberrantly. Expression of DysdsRNA.N.Scer\UAS in the mesodermal tissue (under the control of Scer\GAL4how-24B) does not effect the axon termination process.