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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes

Imprecise excision of the P{EP}Atg1EP3348 insertion resulting in a deletion that extends 966 bp downstream of the insertion site.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Deletion of 966 bases downstream of the P{EP}Atg1EP3348 insertion site, including the first intron of Atg1 which includes the translation start site.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Atg1Δ3D somatic clones in the eye do not lead to loss of photoreceptor cells, as compared to controls.

Homozygous mushroom body gamma neuron clones show normal axon pruning.

Atg1Δ3D/Df(3L)BSC10 animals show disruption of the lamina in the brain optic lobe.

Atg1Δ3D mutant somatic clones generated in the fat body undergo normal endocytosis; endocytic tracer is seen throughout the cytosol of both control and mutant cells.

Atg1Δ3D is able to completely suppress the formation of autophagosomes in the muscles of both untreated and chloroquine-treated larvae starved on low-nutrient food for 6 hours.

Ovarian follicle cell clones of Atg1Δ3D exhibit impaired autophagy induction.

Chimeric ovaries composed from an Atg1Δ3D hemizygous germline and wild-type follicle cells are defective in autophagy, as starvation does not induced lysotracker staining in the mutant germline cells, but in the enveloping wild-type follicle cells. Atg1Δ3D germline chimeras develop functional ovaries, and their egg-laying behavior and hatching rates are indistinguishable from sibling control chimeras, albeit the offspring develop with a delay of 2 days. When the Atg1Δ3D germline chimeras are crossed with Atg1Δ3D heterozygous males, the resulting Atg1Δ3D homozygous mutant animals die in late larval stages, similar to Atg1Δ3D homozygous mutants derived from heterozygous mothers. There are no defects in egg chamber development or egg morphology.

Heat-shock induced mitotic recombination results in Atg1Δ3D homozygous mutant follicle cell clones in 69% of the egg chambers with most of them being mosaic. Flies containing Atg1Δ3D mutant follicle cell clones lay very few eggs that resemble those generated by irradiation, lacking dorsal appendages and embryonic cuticle, and only 5% of the eggs hatched. Approximately 89% of the eggs laid by females containing Atg1Δ3D mutant follicle cell clones exhibit dorsal appendage defects; consequently, only 11% of the chimeric eggs hatched. Defective dorsal appendage formation is only observed in 15% of the eggs containing control clones, and 58% of the control eggs hatched. Given that 15% of the control eggs show egg defects, the frequency of the egg phenotype that is solely due to the Atg1Δ3D deletion (74%) is in accordance with the frequency of follicle cell clones observed in Atg1Δ3D chimeras (69%), suggesting that almost every egg chamber containing Atg1Δ3D mutant follicle cell clones results in defective eggs.

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.

Primary hemocytes dissected from homozygous third instar larvae fail to spread, remaining round in shape.

36% of Atg1Δ3D germ line clone stage 14 egg chambers show persisting nurse cell nuclei. 2% of egg chambers display a dumpless phenotype where nurse cell cytoplasm has not been transferred to the oocyte.

Atg1Δ3D/+ results in a significant decrease in life span as compared to control flies.

Cell death in the germarium of Atg1Δ3D germline clones is reduced to 8.4% (compared to 26% of the control) and to 3.5% for mid-stage egg chambers (compared to 9.7% of the control).

Mutants are viable until pupal stages.

The abundance of Lysotracker-positive foci (a marker for autophagosomes) is strongly reduced in Atg1Δ3D guts from larvae exposed to paraquat-containing food or from starved larvae, compared to wild type larvae under the same conditions.

Fewer apoptotic (TUNEL positive) cells are seen in region two cysts in nutrient-deprived Atg1Δ3D mutant germline clones than are seen in wild type. Degenerating stage eight egg chambers in starved Atg1Δ3D clones show low or no TUNEL-positive staining compared with controls, although nuclear DNA condensation is still observed in these egg chambers.

No mitotic defects are evident in the larval brain and imaginal discs of Atg1Δ3D mutant animals.

In normally fed animals, the size of homozygous Atg1Δ3D clones in the wing disc is not significantly different from their twin spot controls, but in animals grown on medium containing 2μm rapamycin, homozygous Atg1Δ3D clones have a 59% larger average clone size compared to the wild-type twin spot.

Cell size in homozygous clones in the fat body is normal in normally fed animals, but is increased compared to controls under starvation conditions.

Starvation-induced autophagy fails to occur in the larval fat body. Larvae show reduced viability and do not develop beyond pupation. During their period of viability, larvae are hypersensitive to starvation.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by

Atg1Δ3D has lethal | pupal stage phenotype, enhanceable by TorΔP

Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Phenotype Manifest In
Enhanced by
NOT suppressed by
Enhancer of
NOT Enhancer of
Suppressor of

Atg1[+]/Atg1Δ3D is a suppressor | partially of retina | adult stage phenotype of Hsap\MAPTGMR.Ex.PJ

Atg1Δ3D is a suppressor of egg | somatic clone phenotype of Fs(3)Apc1

Atg1[+]/Atg1Δ3D is a suppressor of fat body | second instar larval stage phenotype of Tork17004

Atg1[+]/Atg1Δ3D is a suppressor of vesicle phenotype of Tork17004

Atg1[+]/Atg1Δ3D is a suppressor | partially of nucleus phenotype of Tork17004

NOT Suppressor of
Additional Comments
Genetic Interactions

Clonal expression of AdukScer\UAS.cBa under the control of Scer\GAL4Scer\FRT.Rnor\CD2.Act5C in the fat body of Atg1Δ3D mutants leads to robust formation of Atg8a-positive (or LysoTracker positive) autophagosome vesicles in both fed and starved conditions.

The ability of parkScer\UAS.cGa expressed under the control of Scer\GAL4da.G32 to suppress the Pink1B9 mutant phenotypes of an indented thorax and reduced climbing ability is suppressed if the flies are also mutant for Atg1Δ3D.

The ability of ref(2)PScer\UAS.T:Ivir\HA1 expressed under the control of Scer\GAL4da.G32 to suppress the Pink1B9 mutant phenotypes of an indented thorax and reduced climbing ability is suppressed if the flies are also mutant for Atg1Δ3D.

Females resulting from Atg1Δ3D/Fs(3)Apc irradiated larvae containing homozygous Atg1Δ3D follicle cell clones deposit non-typical Fs(3)Apc eggs that are non-flaccid, but contain short and rudimentary dorsal appendages. Embryonic cuticles do not appear in these eggs and no larvae hatch.

Expression of GugScer\UAS.cCa under the control of Scer\GAL4GMR.PU in Atg1Δ3D mutant eyes fails to rescue cell degeneration.

Expression of Gug75QN.Scer\UAS under the control of Scer\GAL4GMR.PU in Atg1Δ3D mutant eyes fails to rescue cell degeneration.

The modest neuromuscular undergrowth seen upon expression of hiwScer\UAS.fl under the control of Scer\GAL4elav-C155 is enhanced in a Atg1Δ3D heterozygous background.

Heterozygosity for Atg1Δ3D reverts the resistance to paraquat toxicity seen in pucE69/+ animals.

One copy of Atg1Δ3D fails to suppress the Scer\GAL432B-driven PaxScer\UAS.cCa-induced wing blistering.

Tork17004 homozygous animals in a heterozygous Atg1Δ3D genetic background grow faster, and extend their developmental stage to mid/late third instar larval stage. Double homozygous animals survive to mid-late third instar larval stage.

Lipid vesicle aggregation in the fat body of Tork17004 homozygous second/early third instar larvae is suppressed in a heterozygous Atg1Δ3D genetic background.

Tork17004 mutant larvae heterozygous for Atg1Δ3D show a partially rescued cell and nuclear salivary gland size.

The reduced size of Pk61C5 clones in the wing disc is not altered if the clones are also homozygous for Atg1Δ3D.

Atg1Δ3D,TorΔP double mutants show lethality at the embryonic stage.

Xenogenetic Interactions

Expression of Hsap\MAPTScer\UAS.T:Avic\GFP under the control of Scer\GAL4shot-OK307 in Atg1Δ3D/+ heterozygous background leads to moderate thoracic collapse and loss of skeletal muscles, this phenotype is strongly enhanced by combination with a single copy of htt98E2.

The formation of giant autophagic bodies in the retina of adult flies expressing Hsap\MAPTGMR.Ex.PJ is partially suppressed by combination with a single copy of Atg1Δ3D.

Co-expression of parkScer\UAS.cGa is no longer able to suppress the defects in climbing ability and indirect flight muscle structure seen in flies expressing Rnor\Otcd.Scer\UAS under the control of Scer\GAL4da.G32 when the flies are also mutant for Atg1Δ3D.

Atg1Δ3D/+ leads to partial suppression of the lifespan reduction seen in flies expressing Hsap\APPAβ42.Scer\UAS under the control of Scer\GAL4ChAT.7.4.

Complementation and Rescue Data
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Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (12)
References (43)