Among male progeny of rescue crosses that carry both the Adar1F4 mutation and the Adar3.4.Scer\UAS construct, the number of Scer\GAL4Act5C.PI driver flies obtained, expressed as a percentage of the number of control flies lacking a GAL4 driver, is 20%. When these flies carry the Adar3.4.G.Scer\UAS transgene, the percentage of surviving flies is 69%; when flies carry the AdarEA.3.4.Scer\UAS transgene, 72% of flies survive.
Under ideal growth conditions, homozygotes develop into morphologically normal adults with profound behavioural deficits. Mutant males rarely successfully mate with wild-type females. When presented with wild-type or Adar- females, mutant males do not initiate any displays of courtship. Homozygous females can be mated by wild-type males and give rise to morphologically normal hemizygous males which show the mutant adult behavioural defects. Mutant adults show severe neuro-behavioural phenotypes. They show uncoordinated locomotion, occasional tremors and varying degrees of abnormal body posture immediately upon eclosion. Mutant adults spend an inordinate amount of time grooming compared to wild type. This obsessive cleaning is apparent throughout the lifetime of the animal. Mutants are capable of flying and jumping but do so only when repeatedly provoked and then only rarely. Flight in these animals is erratic. Flies recover more slowly from ether anesthesia. They show a strong temperature-dependent of behavioural defects resulting in bouts of paralysis and extreme motor uncoordination at the restrictive temperature. Mutant adults do not have a reduced life span. The behavioural phenotypes become more severe with age and some new phenotypes appear. Tremors increase dramatically such that locomotion is severely compromised in animals beyond day 50. Animals fall over and become increasingly inefficient at righting themselves. Many animals beyond day 30 show circling behaviour that varies from wide circling to circling while standing in place. A majority of animals beyond day 50 show a persistent upheld wing phenotype. Marked asymmetries appear in the animals, manifesting as one upheld wing or leg, extension of one or both back legs and more severe asymmetries in posture. The photoreceptors appear disorganised and extend longitudinally, projecting further to reach the laminar layer in mutants (rather than the more compact, organised retinal structure seen in wild-type flies). Young (1-3 day) mutant brains appear grossly normal. However, lesions appear by day 30 and are distributed randomly in the central brain, optic lobes and retina. The lesions appear as vacuolated regions and are most prevalent in the retina, lamina and optic lobes. Vacuoles appear to increase in size and number with age, and by day 50, animals can be found with extensive brain degeneration.
Adar1F4 has abnormal locomotor behavior | adult stage phenotype, suppressible by Scer\GAL4ChAT.7.4/Hsap\ADARB1UAS.cKa
Adar1F4 has abnormal locomotor behavior | adult stage phenotype, non-suppressible by Hsap\ADARUAS.p110/Scer\GAL4ChAT.7.4
Adar1F4 has abnormal locomotor behavior | adult stage phenotype, non-suppressible by Hsap\ADARUAS.p150/Scer\GAL4ChAT.7.4
Adar1F4 is rescued by Scer\GAL4ChAT.7.4/Adar3.4.UAS
Adar1F4 is partially rescued by Scer\GAL4Act5C.PI/Adar3.4.G.UAS
Adar1F4 is partially rescued by Scer\GAL4Act5C.PI/Adar3.4.UAS
Adar1F4 is partially rescued by Scer\GAL4Act5C.PI/Adar3a.UAS
Adar1F4 is not rescued by Scer\GAL4Act5C.PI/AdarEA.3.4.UAS
Expression of Adar3.4.Scer\UAS under the control of Scer\GAL4Cha.7.4 rescues the locomotor defects seen in Adar1F4 adults.
Expression of Adar3a.Scer\UAS, Adar3.4.Scer\UAS or Adar3.4.G.Scer\UAS, all under the control of Scer\GAL4Act5C.PI, in a Adar1F4 background partially rescues the Adar1F4 mutant phenotype. Adar3.4.Scer\UAS gives the most effective rescue and Adar3.4.G.Scer\UAS gives the least effective of the three transgenes.