FB2025_01 , released February 20, 2025
Allele: Dmel\Atg55cc5
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General Information
Symbol
Dmel\Atg55cc5
Species
D. melanogaster
Name
FlyBase ID
FBal0324972
Feature type
allele
Associated gene
Dmel\Atg5
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class

amorphic allele - molecular evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - molecular evidence

(Kim et al., 2016)
Mutagen
CRISPR/Cas9
(Kim et al., 2016)
Progenitor genotype
Cytology
Description

Deletion in X:7 ,322,242-7,323,716 residues (Drosophila melanogaster R6.06), which deletes 5 out of 6 exons of Atg5 (eliminates over 85% of protein coding sequences including the translation start site).

(Kim et al., 2016)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
deletion
X:7,322,242..7,323,716 [-]
Comment:

A 1475 bp DRISPR-Cas9-mediated deletion that removes 5 of the 6 coding exons of Atg5.

(Kim et al., 2016)
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  hereditary ataxia
      CEA
      (Kim et al., 2016)
      CEA with Hsap\ATG5E122D.UAS.Tag:FLAG
      (Kim et al., 2016)
      Modifiers Based on Experimental Evidence ( 1 )
      Disease
      Interaction
      References
      model of  hereditary ataxia
      is ameliorated by Hsap\ATG5UAS.Tag:FLAG
      (Kim et al., 2016)
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Atg55cc5 homozygotes show a significant increase in viral load upon infection with ZIKV, but not with DCV, as compared to infected heterozygous controls. homozygotes infected with ZIKV have a significantly shorter lifespan than infected heterozygous controls; under non-infected, however, mutants and controls have comparable lifespans.

      (Liu et al., 2018)

      Atg55cc5 homozygous adult guts do not show significant changes in the number of pre-enteroendocrine cells, as compared to heterozygous or wild-type controls.

      (Nagy et al., 2017)

      Atg55cc5 homozygote adults display severe mobility defects in climbing assays, as compared to controls.

      Atg55cc5 homozygotes display increased apoptosis in the middle layer of the medial compartment of adult brains, as compared to controls.

      (Kim et al., 2016)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      Xenogenetic Interactions
      Statement
      Reference

      The mobility defects of adult Atg55cc5 homozygotes are suppressed by the expression of Hsap\ATG5Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4tub.PU, but only partially suppressed by the expression of Hsap\ATG5E122D.Scer\UAS.T:Zzzz\FLAG under the control of the same Scer\GAL4tub.PU.

      The increased apoptosis observed in the adult brain of Atg55cc5 homozygotes is partially suppressed by the Scer\GAL4tub.PU-controlled expression of Hsap\ATG5Scer\UAS.T:Zzzz\FLAG, but not of Hsap\ATG5E122D.Scer\UAS.T:Zzzz\FLAG.

      (Kim et al., 2016)
      Complementation and Rescue Data
      Rescued by

      Atg55cc5 is rescued by Atg5Tag:HA

      (Szabó et al., 2023)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      References (12)