FB2026_02 , released June 18, 2026
Allele: Dmel\Rim103
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General Information
Symbol
Dmel\Rim103
Species
D. melanogaster
Name
FlyBase ID
FBal0287816
Feature type
allele
Associated gene
Dmel\Rim
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
P-element activity
(Muller et al., 2012)
Progenitor genotype
P{EPgy2}RimEY05246
(Muller et al., 2012)
Cytology
Description

Imprecise excision of the progenitor insertion resulting in an internal deletion of part of Rim (the majority of three common exons, including the conserved zinc finger domain, the PDZ domain and the C2A domain are deleted).

(Muller et al., 2012)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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 ( 1 )
      Disease
      Evidence
      References
      model of  autism spectrum disorder
      CEA
      (Genç et al., 2020)
      Modifiers Based on Experimental Evidence ( 1 )
      Disease
      Interaction
      References
      exacerbates  autism spectrum disorder
      modeled by kis1
      (Genç et al., 2020)
      modeled by Chd11
      (Genç et al., 2020)
      model of  autism spectrum disorder
      is exacerbated by Pdk133
      (Genç et al., 2020)
      is exacerbated by wrd104
      (Genç et al., 2020)
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      The neurotransmission across neuromuscular junctions in third instar larvae, assessed by excitatory junction potential amplitude and quantal content, is significantly impaired in Rim103/RimEx73 transheterozygotes, but not in Rim103 heterozygotes, as compared to controls.

      (Bruckner et al., 2017)

      Neuromuscular junctions in homozygous third instar larvae show a complete lack of synaptic homeostasis after treatment with philanthotoxin-433 (PhTX): the average EPSP amplitude is significantly reduced in the presence of PhTX compared with the baseline measured in the absence of PhTX. The defect in homeostatic plasticity is not restored by increasing extracellular Ca[2+].

      The neuromuscular junction of mutant third instar larvae shows a significant reduction in EPSC amplitude in response to a single presynaptic stimulus than controls. This relative decrease in EPSC amplitude persists in the mutants at elevated extracellular Ca[2+] levels. Upon repeated stimulation the mutant neuromuscular junctions show very strong facilitation compared to wild type.

      The electrophysiological responses of neuromuscular junctions of mutant third instar larvae are more sensitive to EGTA than wild-type.

      (Muller et al., 2012)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      The neurotransmission across neuromuscular junctions of FifeAC,Rim103 double heterozygous third instar larvae, assessed by excitatory junction potential amplitude and quantal content, is significantly impaired as compared to controls.

      (Bruckner et al., 2017)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (5)
      References (9)