FB2024_03 , released June 25, 2024
Allele: Dmel\Atg125
Open Close
General Information
Symbol
Dmel\Atg125
Species
D. melanogaster
Name
FlyBase ID
FBal0220538
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
unc-5125
Key Links
Genomic Maps

Nature of the Allele
Cytology
Description

Imprecise excision of P{EP}Atg1EP3348has deleted 1787bp downstream from the insertion point.

Imprecise excision of the insertion in Atg1EP3348, resulting in a deletion of 1787bp downstream from the insertion point.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

Imprecise excision of the P{EP}Atg1EP3348 insertion resulting in a deletion that extends 1787 bp downstream of the insertion site.

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
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

Atg125 mutants display basal autophagy defects in larval fat body cells.

Atg125 homozygous third instar larval mushroom bodies show prevalent disintegration of the core into multiple bundles and defects in the extension of calix dendrites, as compared to controls. The mutants mushroom bodies also show defective axonal transport of the synaptic vesicle (monitored by the localization of nSyb::GFP and Syt::eGFP ) despite of no obvious defects in microtubule integrity (assessed by the pattern of Tau::GFP and Futsch), and show aberrant accumulation of early endosomes, late endosomes and Golgi apparatus in the cell body, calyx and lobes, but no defects in the localization of autophagosomes or of mitochondria, as compared to controls.

Marker analysis indicates that pre-and post synaptic component of the neuromuscular junction fail to align properly in Atg125 homozygous or Atg125/Atg13 heterozygous larvae.

Atg13/Atg125 and Atg125/Df(3L)ED4486 animals show axonal transport defects at the larval stage.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressor of
Statement
Reference

Atg125, maskUAS.cZa, Atg1[+], Scer\GAL4how-24B is a suppressor | partially of pupal thorax | heat sensitive phenotype of ProsĪ²61.B.UAS, Scer\GAL4how-24B

NOT Suppressor of
Statement
Reference

Atg125/Atg13 is a non-suppressor of neuroblast | larval stage phenotype of fzy1/fzy5032

Other
Additional Comments
Genetic Interactions
Statement
Reference

Atg125/Atg13 does not suppress the neuroblast loss seen in fzy5032/fzy1 mutant larval brains.

Atg125, Klc8ex94 heterozygous third instar larval mushroom bodies show defects in the extension of calix dendrites, but no obvious core integrity, as compared to either heterozygous controls.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by

Atg125 is partially rescued by Atg1UAS.cTa

Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)