Stop codon after amino acid 278.
Mutation within AdoR.
Feeding wild-type flies with the adenosine receptor agonist CADO (2-chloroadenosine) leads to developmental delays as well as larval and pupal lethality. AdoR1 mutants are resistant to CADO treatment.
Compared with wild-type, AdoR1 mutants display reduced performance in associative learning.
Synaptic strength and plasticity at the neuromuscular junction (NMJ) are impaired in AdoR1 third instar larvae. Excitatory junction potentials (EJPs) are significantly elevated in AdoR1 mutants compared with wild-type. The amplitude of spontaneous miniature excitatory junction potentials (mEJPs) is not significantly different in AdoR1 mutants and wild-type controls. Compared with wild-type, AdoR1 mutants show a reduction in paired-pulse plasticity at short interstimulus intervals. The amplitude of stimulus induced calcium transients is elevated in AdoR1 mutants relative to wild-type. The increased amplitude of calcium transients in AdoR1 mutants is attributable to an increase in calcium influx rather than impaired calcium extrusion.
AdoR1 has abnormal starvation stress response phenotype, suppressible by Akh1/Akh1
AdoR1 is a non-enhancer of abnormal learning | recessive phenotype of Ent2P124
AdoR1 is a non-enhancer of abnormal learning | recessive phenotype of Ent23
AdoR1/AdoR1 is a suppressor of abnormal starvation stress response phenotype of Akh1
AdoR1 is a suppressor of abnormal neurophysiology | recessive | third instar larval stage phenotype of Ent23
AdoR1 is a suppressor of abnormal neurophysiology | recessive | third instar larval stage phenotype of Ent2P124
AdoR1 is a suppressor | partially of abnormal developmental rate phenotype of Dp(3;3)Karel
AdoR1 is a suppressor | partially of lethal phenotype of Dp(3;3)Karel
AdoR1 is a suppressor | partially of melanotic mass phenotype phenotype of Dp(3;3)Karel
AdoR1 is a non-suppressor of abnormal learning | recessive phenotype of Ent23
AdoR1 is a non-suppressor of abnormal learning | recessive phenotype of Ent2P124
AdoR1, Akh1 has abnormal oxidative stress response phenotype
AdoR1 is a suppressor | partially of melanotic mass phenotype of Dp(3;3)Karel
AdoR1 is a suppressor of embryonic/larval crystal cell phenotype of Dp(3;3)Karel
AdoR1 is a suppressor | partially of lamellocyte phenotype of Dp(3;3)Karel
AdoR1 is a non-suppressor of embryonic/larval fat body phenotype of Dp(3;3)Karel
Akh1/Akh1;AdoR1/AdoR1 double mutants have similar mortality rates to wild type flies under starvation conditions. Akh1/Akh1;AdoR1/AdoR1 double mutants have significantly higher mortality rates than controls in response to 20mM paraquat (Akh1/Akh1 single mutants are similar to wild type and AdoR1/AdoR1 single mutants show resistance to paraquat).
The performance index of Ent2P124, AdoR1 double mutants in associative learning is not significantly different from the performance indices of either the Ent2P124 of AdoR1 single mutants.
The performance index of Ent23, AdoR1 double mutants in associative learning is not significantly different from the performance indices of either the Ent23 of AdoR1 single mutants.
The synaptic defects observed in either Ent2P124 or AdoR1 single mutants are suppressed in Ent2P124, AdoR1 double mutants. EJP amplitudes are not significantly different in the double mutant and wild-type controls. Ent2P124, AdoR1 double mutants also show normal paired-pulse facilitation and calcium influx.
The synaptic defects observed in either Ent23 or AdoR1 single mutants are suppressed in Ent23, AdoR1 double mutants. EJP amplitudes are not significantly different in the double mutant and wild-type controls. Ent23, AdoR1 double mutants also show normal paired-pulse facilitation and calcium influx.
Introduction of the AdoR1 mutation significantly increases pupariation and the adult emerging rate in Dp(3;3)Karel mutants. Developmental delay in the double mutant larvae is much less pronounced than in the Dp(3;3)Karel single mutant, with most of the double mutant larvae pupariating within 1 day after their control siblings. The disintegration of the fat body seen in Dp(3;3)Karel larvae is not altered by introduction of AdoR1, but the formation of melanotic tumours is significantly reduced. The total number of circulating hemocytes is not significantly changed in the double mutant larvae compared to Dp(3;3)Karel single mutants, but the number of lamellocytes is decreased and the number of crystal cells is normal.