FB2025_01 , released February 20, 2025
Allele: Dmel\AdoR1
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General Information
Symbol
Dmel\AdoR1
Species
D. melanogaster
Name
FlyBase ID
FBal0191589
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Associated Insertion(s)
Cytology
Description

Stop codon after amino acid 278.

Mutation within AdoR.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
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Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

AdoR1/AdoR1 5 day old males show significantly increased mortality under starvation conditions compared to controls. AdoR1/AdoR1 flies show significant resistance (lower mortality rates) to paraquat toxicity (20mM) compared to wild type.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
NOT Enhancer of
Statement
Reference

AdoR1 is a non-enhancer of abnormal learning | recessive phenotype of Ent2P124

AdoR1 is a non-enhancer of abnormal learning | recessive phenotype of Ent23

Suppressor of
NOT Suppressor of
Statement
Reference

AdoR1 is a non-suppressor of viable phenotype of Ent23

AdoR1 is a non-suppressor of abnormal learning | recessive phenotype of Ent23

AdoR1 is a non-suppressor of viable phenotype of Ent2P124

AdoR1 is a non-suppressor of abnormal learning | recessive phenotype of Ent2P124

Other
Phenotype Manifest In
Suppressor of
Statement
Reference

AdoR1 is a suppressor of synapse phenotype of Ent23

AdoR1 is a suppressor of synapse phenotype of Ent2P124

AdoR1 is a suppressor | partially of lamellocyte phenotype of Dp(3;3)Karel

NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

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.

Xenogenetic Interactions
Statement
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Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (7)