FB2025_01 , released February 20, 2025
Allele: Dmel\Atg13Δ81
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General Information
Symbol
Dmel\Atg13Δ81
Species
D. melanogaster
Name
FlyBase ID
FBal0221508
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
atg1381
Key Links
Nature of the Allele
Cytology
Description

Imprecise excision of the progenitor insertion, resulting in a deletion that removes 593bp including the translation start site and the first 104 codons of Atg13.

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
References
Modifiers Based on Experimental Evidence ( 1 )
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

Atg13Δ81 homozygous clones in mosaic third instar larval eye-antennal imaginal discs occupy a significantly smaller proportion of the disc area and result in decreased eye sizes in adults, as compared to control clones.

Third larval instar eye-antennal discs have normal morphology.

The kinetics of the clearance of the paternal mitochondrial derivatives is normal in embryos derived from females carrying Atg13Δ81 germline clones.

Atg13Δ81 mutants display basal autophagy defects in larval fat body cells.

Heat-shock induced Atg13Δ81 follicle cell clones generate eggs where approximately 42% exhibit dorsal appendage defects and 34% hatch.

Atg13Δ74/Atg13Δ81 mutant mosaic germline cells are defective in autophagy (as monitored by the lack of lysotracker staining). However, the chimeras are fully fertile with normal egg-laying behavior and hatching rates. There are no defects in egg chamber development or egg morphology. These germline mosaics do not show disruption of nurse cell apoptosis.

Females carrying homozygous germline clones have a significant increase in the number of stage 14 egg chambers that have persisting TUNEL-negative nurse cell nuclei compared to wild-type egg chambers at the same stage, in which nurse cell nuclei are rarely detected (and those that are detected are all TUNEL positive). The persisting nurse cell nuclei show condensed nuclear staining.

Homozygous clones in the larval fat body fail to induce autophagy in response to treatment with rapamycin.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Suppressor of
Statement
Reference
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

scrib673-homozygous, Ras85DV12.Scer\UAS-expressing eye-antennal imaginal disc clone tumors are significantly suppressed by Atg13Δ81 homozygosity in clone cells (leading to reductions in the proportions of clone cells entering the cell cycle, but not undergoing mitosis or apoptosis, and leading to a reduction in the tumor size, but not invasiveness), in neighboring disc cells (leading to reductions in the tumor size and in the proportion of cell entering the cell cycle, but not undergoing mitosis or apoptosis), in the full organism except the clone cells (leading to reductions in the tumor size and invasiveness), or in the full organism (leading to reductions in the proportions of cells entering the cell cycle, undergoing mitosis, but not undergoing apoptosis, and leading to reductions in the tumor size and invasiveness); these scrib673-homozygous, Ras85DV12.Scer\UAS-expressing tumors are also significantly suppressed by the combination of Atg13Δ81 homozygosity in the tumor cells and Atg14Δ5.2 homozygosity in the neighboring disc cells. One copy of Atg13+tCH322-168O18 in the full organism suppresses the decrease in tumor size, but not the decrease in invasiveness, resulting from Atg13Δ81 homozygosity either in the full organism or in the full organism apart from clone cells; one copy of Atg13ey.3.5 in the full organism also partially suppresses the decrease in tumor size resulting from Atg13Δ81 homozygosity. These scrib673-homozygous, Ras85DV12.Scer\UAS-expressing tumors grow to significantly smaller sizes when grafted into the abdomen of either Atg14Δ5.2/Atg14EY14568 transheterozygous adult hosts (but not if hosts also possess one copy of Atg14+tCH322-175F03) or Atg8ad4 homozygous adult hosts, as compared to control hosts.

The cell non-autonomous increase in autophagosomes resulting from the presence of clones homozygous for scrib673 and expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU in third instar larval eye-antennal imaginal discs is suppressed by Atg13Δ81 homozygosity in either the full organism (leading to suppression in distant tissues - somatic muscles, midgut and fat body) or in the full organism apart from the clone cells (leading to suppression in neighboring disc tissue).

Atg13Δ81 homozygosity in neighboring disc tissue does not significantly change the size of third instar larval eye-antennal imaginal disc tumors resulting from the clonal expression of ykiS168A.Scer\UAS.T:Avic\GFP-EGFP,T:Ivir\HA1 under the control of Scer\GAL4Act.PU.

The robust formation of Atg8a-positive (or LysoTracker positive) autophagosome vesicles the AdukScer\UAS.cBa-expressing (controlled by Scer\GAL4Scer\FRT.Rnor\CD2.Act5C) fat body clones in fed larvae is not observed when the clones are induced in Atg13Δ81 mutant background.

The autophagy that is induced by expression of bskScer\UAS.cBa under the control of Scer\GAL4Act in clones in the larval fat body still occurs in an Atg13Δ81 homozygous background.

Xenogenetic Interactions
Statement
Reference

Expression of Hsap\MAPTScer\UAS.T:Avic\GFP under the Scer\GAL4shot-OK307 driver in adults heterozygous for Atg13Δ81 has no phenotype, unless the animals are also heterozygous for htt98E2, in which case a severe loss of thoracic somatic muscles is observed.

Complementation and Rescue Data
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Mutant
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Stocks (0)
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (18)