FB2026_02 , released June 18, 2026
Allele: Dmel\fusl1
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General Information
Symbol
Dmel\fusl1
Species
D. melanogaster
Name
FlyBase ID
FBal0218988
Feature type
allele
Associated gene
Dmel\fusl
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
(Long et al., 2008)
Progenitor genotype
Cytology
Description

Nucleotide substitution: T?A.

(Long et al., 2008)

Amino acid replacement: C89term.

(Long et al., 2008)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2L:5,332,148..5,332,148 [-]
Nucleotide change:

T5332148A

Reported nucleotide change:

T?A

Amino acid change:

C89term | fusl-PA; C89term | fusl-PB; C89term | fusl-PC; C89term | fusl-PD; C89term | fusl-PE; C89term | fusl-PF

Reported amino acid change:

C89term

(Long et al., 2008)
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 ( 0 )
      Disease
      Evidence
      References
      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

      Mutant flies have an abnormal electroretinogram; the sustained photoreceptor component is normal in amplitude and duration, but the synaptic on- and off-transients are absent. Intracellular recordings from mutant photoreceptors indicate that the photoreceptor potentials have normal amplitude and duration, but they have ab aberrant, slowly decaying component.

      Mutant third instar larvae do not show any detectable defects in the gross architecture of the musculature, with normal motor nerve trajectories, normal muscle anatomy and normally placed and differentiated neuromuscular junctions.

      Homozygous and hemizygous larvae show a highly significant reduction in pharyngeal movements and locomotor body wall contractions compared to controls.

      Homozygous and hemizygous larvae show a significant decrease in mean evoked EJC amplitude at the neuromuscular junction. The mutants show a significant increase in both the amplitude and frequency of mEJC events. Homozygous and hemizygous larvae show a significant impairment of endo-exo synaptic vesicle cycling (assayed by lipophilic dye imaging), with a particularly severe defect in synaptic vesicle exocytosis. The mutants display insensitivity to increasing concentrations of Ca[2+] compared to controls, with only small increases in EJC amplitude.

      Ultrastructurally, the overall synapse structure appears normal in mutant larvae. The presynaptic boutons are normal in size and contain the expected array of organelles, with well differentiated presynaptic and postsynaptic membrane profiles. Synaptic vesicles are normal in size, but there is a dramatic elevation of vesicle number throughout the bouton and also clustered around presynaptic active zones in the mutants. The number of synaptic vesicles physically docked at the presynaptic active zone densities is also very significantly increased compared to controls.

      (Long et al., 2008)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      NOT suppressed by
      Statement
      Reference

      fusl1 has abnormal neurophysiology phenotype, non-suppressible by cacUAS.EGFP/Scer\GAL4elav.PLu

      (Long et al., 2008)
      Phenotype Manifest In
      NOT suppressed by
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      The defects in mean EJC amplitude seen at the neuromuscular junction in fusl1 larvae are not rescued by expression of cacScer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4elav.PLu.

      (Long et al., 2008)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      fusl1 is rescued by fuslUAS.EGFP/Scer\GAL4elav.PLu

      (Long et al., 2008)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer

      Selected as: a mutation with an abnormal electroretinogram response.

      (Long et al., 2008)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (1)
      Reported As
      Symbol Synonym
      fusl1
      (Long et al., 2008)
      Name Synonyms
      Secondary FlyBase IDs
        References (1)