FlyBase Allele Report: Dmel\Atg1[Δ3D]

General Information

Symbol

Dmel\Atg1^Δ3D

Species

D. melanogaster

Name

FlyBase ID

FBal0176392

Feature type

allele

Associated gene

Dmel\Atg1

Associated Insertion(s)

Carried in Construct

Also Known As

Atg1Δ3D

Genomic Maps

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Allele class

loss of function allele

Mutagen

P-element activity

Nature of the Allele

Allele class

loss of function allele

(Scott et al., 2007, Scott et al., 2004)

Mutagen

P-element activity

(Scott et al., 2004)

Mutations Mapped to the Genome

Type

Location

Additional Notes

References

deletion

3L:12,804,017..12,804,983 [-]

Comment:

Imprecise excision of the P{EP}Atg1^EP3348 insertion resulting in a deletion that extends 966 bp downstream of the insertion site.

(Scott et al., 2004)

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Progenitor genotype

Atg1^EP3348

(Scott et al., 2004)

Cytology

Nature of the lesion

Statement

Reference

Deletion of 966 bases downstream of the P{EP}Atg1^EP3348 insertion site, including the first intron of Atg1 which includes the translation start site.

(Scott et al., 2004)

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

ameliorates tauopathy

modeled by Hsap\MAPT^GMR.Ex.PJ

(Bakhoum et al., 2014)

ameliorates Alzheimer's disease

modeled by Hsap\APP^{Aβ42.UAS.Tag:SS(rPENK)}

(Ling et al., 2009)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Phenotypic Data

Phenotypic Class

cell death defective | germline clone

(Barth et al., 2011)

cell death defective | germline clone | oogenesis stage S14

(Bass et al., 2009)

cell death defective | somatic clone

(Barth et al., 2011)

decreased cell death | adult stage | germline clone | nutrition conditional

(Hou et al., 2008)

decreased cell death | somatic clone

(Nezis et al., 2009)

developmental rate defective | germline clone

(Barth et al., 2011)

lethal - all die before end of larval stage | germline clone

(Barth et al., 2011)

lethal - all die before end of pupal stage

(Scott et al., 2004)

lethal - all die before end of pupal stage | recessive

(Scott et al., 2007)

lethal - all die during pupal stage

(Wu et al., 2009)

neuroanatomy defective (with Df(3L)BSC10)

(Kim et al., 2013)

oxidative stress response defective | third instar larval stage

(Wu et al., 2009)

short lived | dominant

(Ling et al., 2009)

some die during larval stage | germline clone

(Barth et al., 2011)

some die during pupal stage

(Scott et al., 2004)

some die during pupal stage | recessive

(Scott et al., 2007)

starvation stress response defective

(Zirin et al., 2013)

starvation stress response defective | third instar larval stage

(Wu et al., 2009)

Phenotype Manifest In

autophagosome | :chemical conditional | nutrition conditional

(Zirin et al., 2013)

autophagosome | nutrition conditional

(Zirin et al., 2013)

autophagosome | third instar larval stage | chemical conditional

(Wu et al., 2009)

dorsal appendage | somatic clone

(Barth et al., 2011)

egg | somatic clone

(Barth et al., 2011)

egg chamber | germline clone | nutrition conditional

(Hou et al., 2008)

egg chamber | germline clone | oogenesis stage S14

(Bass et al., 2009)

egg chamber | somatic clone

(Nezis et al., 2009)

embryonic/larval cuticle | somatic clone

(Barth et al., 2011)

embryonic/larval gut | third instar larval stage | chemical conditional, with Scer\GAL4^Act5C.PP

(Wu et al., 2009)

embryonic/larval hemocyte

(Velichkova et al., 2010)

fat body

(Scott et al., 2004)

female germline cyst | germline clone | nutrition conditional

(Hou et al., 2008)

germarium | somatic clone

(Nezis et al., 2009)

germarium region 2 | germline clone | nutrition conditional

(Hou et al., 2008)

lamina (with Df(3L)BSC10)

(Kim et al., 2013)

nurse cell | germline clone | oogenesis stage S14

(Nezis et al., 2010, Bass et al., 2009)

Detailed Description

Statement

Reference

Atg1^Δ3D somatic clones in the eye do not lead to loss of photoreceptor cells, as compared to controls.

(Robin et al., 2019)

Homozygous mushroom body gamma neuron clones show normal axon pruning.

(Issman-Zecharya and Schuldiner, 2014)

Atg1^Δ3D/Df(3L)BSC10 animals show disruption of the lamina in the brain optic lobe.

(Kim et al., 2013)

Atg1^Δ3D mutant somatic clones generated in the fat body undergo normal endocytosis; endocytic tracer is seen throughout the cytosol of both control and mutant cells.

(Shravage et al., 2013)

Atg1^Δ3D 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.

(Zirin et al., 2013)

Ovarian follicle cell clones of Atg1^Δ3D exhibit impaired autophagy induction.

Chimeric ovaries composed from an Atg1^Δ3D 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. Atg1^Δ3D 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 Atg1^Δ3D germline chimeras are crossed with Atg1^Δ3D heterozygous males, the resulting Atg1^Δ3D homozygous mutant animals die in late larval stages, similar to Atg1^Δ3D homozygous mutants derived from heterozygous mothers. There are no defects in egg chamber development or egg morphology.

Heat-shock induced mitotic recombination results in Atg1^Δ3D homozygous mutant follicle cell clones in 69% of the egg chambers with most of them being mosaic. Flies containing Atg1^Δ3D 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 Atg1^Δ3D 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 Atg1^Δ3D deletion (74%) is in accordance with the frequency of follicle cell clones observed in Atg1^Δ3D chimeras (69%), suggesting that almost every egg chamber containing Atg1^Δ3D mutant follicle cell clones results in defective eggs.

(Barth et al., 2011)

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.

(Nezis et al., 2010)

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

(Velichkova et al., 2010)

36% of Atg1^Δ3D 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.

(Bass et al., 2009)

Atg1^Δ3D/+ results in a significant decrease in life span as compared to control flies.

(Ling et al., 2009)

Cell death in the germarium of Atg1^Δ3D 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).

(Nezis et al., 2009)

Mutants are viable until pupal stages.

The abundance of Lysotracker-positive foci (a marker for autophagosomes) is strongly reduced in Atg1^Δ3D guts from larvae exposed to paraquat-containing food or from starved larvae, compared to wild type larvae under the same conditions.

(Wu et al., 2009)

Fewer apoptotic (TUNEL positive) cells are seen in region two cysts in nutrient-deprived Atg1^Δ3D mutant germline clones than are seen in wild type. Degenerating stage eight egg chambers in starved Atg1^Δ3D clones show low or no TUNEL-positive staining compared with controls, although nuclear DNA condensation is still observed in these egg chambers.

(Hou et al., 2008)

No mitotic defects are evident in the larval brain and imaginal discs of Atg1^Δ3D mutant animals.

(Lee et al., 2007)

In normally fed animals, the size of homozygous Atg1^Δ3D clones in the wing disc is not significantly different from their twin spot controls, but in animals grown on medium containing 2μm rapamycin, homozygous Atg1^Δ3D 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.

(Scott et al., 2007)

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.

(Scott et al., 2004)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Atg1^Δ3D has lethal | pupal stage phenotype, enhanceable by Tor^ΔP

(Scott et al., 2004)

Enhancer of

Statement

Reference

Atg1^Δ3D/Atg1^Δ3D is an enhancer | somatic clone of decreased cell number | adult stage phenotype of Scer\GAL4^ninaE.PT, p53^UAS.Dp53

(Robin et al., 2019)

Atg1^Δ3D is an enhancer of neuroanatomy defective phenotype of Scer\GAL4^elav-C155, hiw^UAS.fl

(Shen and Ganetzky, 2009)

Atg1^Δ3D is an enhancer of decreased cell growth phenotype of Scer\GAL4^elav-C155, hiw^UAS.fl

(Shen and Ganetzky, 2009)

Atg1^Δ3D is an enhancer of lethal | larval stage phenotype of Tor^ΔP

(Scott et al., 2004)

NOT Enhancer of

Statement

Reference

Atg1^Δ3D/Atg1^Δ3D is a non-enhancer | somatic clone of decreased cell number | adult stage phenotype of Scer\GAL4^ninaE.PT, p53^UAS.DΔNp53

(Robin et al., 2019)

Suppressor of

Statement

Reference

Atg1[+]/Atg1^Δ3D is a suppressor of short lived phenotype of Hsap\APP^{Aβ42.Scer\UAS.T:Rnor\SS-PENK}/Hsap\APP^{Aβ42.UAS.Tag:SS(rPENK)}

(Ling et al., 2009)

Atg1[+]/Atg1^Δ3D is a suppressor of oxidative stress response defective | dominant phenotype of puc^E69

(Wu et al., 2009)

Atg1[+]/Atg1^Δ3D is a suppressor of body size defective | second instar larval stage phenotype of Tor^k17004

(Lee et al., 2007)

Atg1[+]/Atg1^Δ3D is a suppressor | partially of decreased cell size phenotype of Tor^k17004

(Lee et al., 2007)

Atg1^Δ3D/Atg1^Δ3D is a suppressor of body size defective | second instar larval stage phenotype of Tor^k17004

(Lee et al., 2007)

Atg1^Δ3D/Atg1^Δ3D is a suppressor | partially of lethal phenotype of Tor^k17004

(Lee et al., 2007)

NOT Suppressor of

Statement

Reference

Atg1^Δ3D/Atg1^Δ3D is a non-suppressor | somatic clone of decreased cell number | adult stage phenotype of Scer\GAL4^ninaE.PT, p53^UAS.DΔNp53

(Robin et al., 2019)

Atg1[+]/Atg1^Δ3D is a non-suppressor of visible phenotype of Pax^UAS.cCa, Scer\GAL4^32B

(Chen et al., 2008)

Phenotype Manifest In

Enhanced by

Statement

Reference

Atg1[+]/Atg1^Δ3D, Hsap\MAPT^UAS.GFP, Scer\GAL4^shot-OK307 has adult thorax phenotype, enhanceable by htt^98E2/htt[+]

(Rui et al., 2015)

Atg1[+]/Atg1^Δ3D, Hsap\MAPT^UAS.GFP, Scer\GAL4^shot-OK307 has skeletal muscle of thorax phenotype, enhanceable by htt^98E2/htt[+]

(Rui et al., 2015)

NOT suppressed by

Statement

Reference

Atg1^Δ3D has eye | somatic clone phenotype, non-suppressible by Gug^UAS.cCa/Scer\GAL4^GMR.PU

(Nisoli et al., 2010)

Atg1^Δ3D has eye | somatic clone phenotype, non-suppressible by Gug^75QN.UAS/Scer\GAL4^GMR.PU

(Nisoli et al., 2010)

Enhancer of

Statement

Reference

Atg1^Δ3D/Atg1^Δ3D is an enhancer | somatic clone of eye photoreceptor cell phenotype of Scer\GAL4^ninaE.PT, p53^UAS.Dp53

(Robin et al., 2019)

Atg1^Δ3D is an enhancer of neuromuscular junction phenotype of Scer\GAL4^elav-C155, hiw^UAS.fl

(Shen and Ganetzky, 2009)

NOT Enhancer of

Statement

Reference

Atg1^Δ3D/Atg1^Δ3D is a non-enhancer | somatic clone of eye photoreceptor cell phenotype of Scer\GAL4^ninaE.PT, p53^UAS.DΔNp53

(Robin et al., 2019)

Zzzz\Poly-Ala^{A37.UAS.EGFP,Tag:NLS(SV40-largeT)}, Atg1[+], Atg1^Δ3D is a non-enhancer of eye phenotype of Zzzz\Poly-Ala^{A37.UAS.EGFP,Tag:NLS(SV40-largeT)}/Scer\GAL4^ey.PB, Zzzz\Poly-Ala^{A37.Scer\UAS.T:Avic\GFP-EGFP,T:SV40\nls2}

(Berger et al., 2006)

Suppressor of

Statement

Reference

Atg1[+]/Atg1^Δ3D is a suppressor | partially of retina | adult stage phenotype of Hsap\MAPT^GMR.Ex.PJ

(Bakhoum et al., 2014)

Atg1[+]/Atg1^Δ3D is a suppressor | partially of autophagosome | adult stage phenotype of Hsap\MAPT^GMR.Ex.PJ

(Bakhoum et al., 2014)

Atg1^Δ3D is a suppressor of dorsal appendage | somatic clone phenotype of Fs(3)Apc¹

(Barth et al., 2011)

Atg1^Δ3D is a suppressor of embryonic/larval cuticle | somatic clone phenotype of Fs(3)Apc¹

(Barth et al., 2011)

Atg1^Δ3D is a suppressor of egg | somatic clone phenotype of Fs(3)Apc¹

(Barth et al., 2011)

Atg1[+]/Atg1^Δ3D is a suppressor of fat body | second instar larval stage phenotype of Tor^k17004

(Lee et al., 2007)

Atg1[+]/Atg1^Δ3D is a suppressor of vesicle phenotype of Tor^k17004

(Lee et al., 2007)

Atg1[+]/Atg1^Δ3D is a suppressor | partially of nucleus phenotype of Tor^k17004

(Lee et al., 2007)

NOT Suppressor of

Statement

Reference

Atg1^Δ3D/Atg1^Δ3D is a non-suppressor | somatic clone of eye photoreceptor cell phenotype of Scer\GAL4^ninaE.PT, p53^UAS.DΔNp53

(Robin et al., 2019)

Atg1^Δ3D is a non-suppressor of autophagosome | somatic clone | larval stage phenotype of Aduk^UAS.cBa, Scer\GAL4^{FRT.Rnor\Cd2.Act5C}

(Braden and Neufeld, 2016)

Atg1^Δ3D is a non-suppressor of embryonic/larval fat body | somatic clone | larval stage phenotype of Aduk^UAS.cBa, Scer\GAL4^{FRT.Rnor\Cd2.Act5C}

(Braden and Neufeld, 2016)

Atg1[+]/Atg1^Δ3D is a non-suppressor of wing phenotype of Pax^UAS.cCa, Scer\GAL4^32B

(Chen et al., 2008)

Atg1^Δ3D is a non-suppressor of wing disc | somatic clone phenotype of Pdk1⁵

(Scott et al., 2007)

Other

Statement

Reference

Atg1[+]/Atg1^Δ3D, Hsap\MAPT^UAS.GFP, Scer\GAL4^shot-OK307 has adult thorax phenotype

(Rui et al., 2015)

Atg1[+]/Atg1^Δ3D, Hsap\MAPT^UAS.GFP, Scer\GAL4^shot-OK307 has skeletal muscle of thorax phenotype

(Rui et al., 2015)

Atg1^Δ3D, Fs(3)Apc¹ has dorsal appendage | somatic clone phenotype

(Barth et al., 2011)

Atg1^Δ3D, Fs(3)Apc¹ has embryonic/larval cuticle | somatic clone phenotype

(Barth et al., 2011)

Atg1^Δ3D, Fs(3)Apc¹ has egg | somatic clone phenotype

(Barth et al., 2011)

Additional Comments

Genetic Interactions

Statement

Reference

Clonal expression of Aduk^Scer\UAS.cBa under the control of Scer\GAL4^{Scer\FRT.Rnor\CD2.Act5C} in the fat body of Atg1^Δ3D mutants leads to robust formation of Atg8a-positive (or LysoTracker positive) autophagosome vesicles in both fed and starved conditions.

(Braden and Neufeld, 2016)

The ability of park^Scer\UAS.cGa expressed under the control of Scer\GAL4^da.G32 to suppress the Pink1^B9 mutant phenotypes of an indented thorax and reduced climbing ability is suppressed if the flies are also mutant for Atg1^Δ3D.

The ability of ref(2)P^{Scer\UAS.T:Ivir\HA1} expressed under the control of Scer\GAL4^da.G32 to suppress the Pink1^B9 mutant phenotypes of an indented thorax and reduced climbing ability is suppressed if the flies are also mutant for Atg1^Δ3D.

(de Castro et al., 2013)

Females resulting from Atg1^Δ3D/Fs(3)Apc irradiated larvae containing homozygous Atg1^Δ3D 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.

(Barth et al., 2011)

Expression of Gug^Scer\UAS.cCa under the control of Scer\GAL4^GMR.PU in Atg1^Δ3D mutant eyes fails to rescue cell degeneration.

Expression of Gug^{75QN.Scer\UAS} under the control of Scer\GAL4^GMR.PU in Atg1^Δ3D mutant eyes fails to rescue cell degeneration.

(Nisoli et al., 2010)

The modest neuromuscular undergrowth seen upon expression of hiw^Scer\UAS.fl under the control of Scer\GAL4^elav-C155 is enhanced in a Atg1^Δ3D heterozygous background.

(Shen and Ganetzky, 2009)

Heterozygosity for Atg1^Δ3D reverts the resistance to paraquat toxicity seen in puc^E69/+ animals.

(Wu et al., 2009)

One copy of Atg1^Δ3D fails to suppress the Scer\GAL4^32B-driven Pax^Scer\UAS.cCa-induced wing blistering.

(Chen et al., 2008)

Tor^k17004 homozygous animals in a heterozygous Atg1^Δ3D 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 Tor^k17004 homozygous second/early third instar larvae is suppressed in a heterozygous Atg1^Δ3D genetic background.

Tor^k17004 mutant larvae heterozygous for Atg1^Δ3D show a partially rescued cell and nuclear salivary gland size.

(Lee et al., 2007)

The reduced size of Pk61C⁵ clones in the wing disc is not altered if the clones are also homozygous for Atg1^Δ3D.

(Scott et al., 2007)

Atg1^Δ3D,Tor^ΔP double mutants show lethality at the embryonic stage.

(Scott et al., 2004)

Xenogenetic Interactions

Statement

Reference

Expression of Hsap\MAPT^{Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^shot-OK307 in Atg1^Δ3D/+ heterozygous background leads to moderate thoracic collapse and loss of skeletal muscles, this phenotype is strongly enhanced by combination with a single copy of htt^98E2.

(Rui et al., 2015)

The formation of giant autophagic bodies in the retina of adult flies expressing Hsap\MAPT^GMR.Ex.PJ is partially suppressed by combination with a single copy of Atg1^Δ3D.

(Bakhoum et al., 2014)

Co-expression of park^Scer\UAS.cGa is no longer able to suppress the defects in climbing ability and indirect flight muscle structure seen in flies expressing Rnor\Otc^d.Scer\UAS under the control of Scer\GAL4^da.G32 when the flies are also mutant for Atg1^Δ3D.

(Pimenta de Castro et al., 2012)

Atg1^Δ3D/+ leads to partial suppression of the lifespan reduction seen in flies expressing Hsap\APP^{Aβ42.Scer\UAS} under the control of Scer\GAL4^ChAT.7.4.

(Ling et al., 2009)

Complementation and Rescue Data

Rescued by

Atg1^Δ3D is rescued by Atg1^UAS.cSa/Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Partially rescued by

Atg1^Δ3D is partially rescued by Scer\GAL4^hs.PH/Atg1^UAS.cSa

(Scott et al., 2007)

Atg1^Δ3D is partially rescued by Scer\GAL4^hs.PH/Atg1^UAS.cSa

(Scott et al., 2007)

Atg1^Δ3D is partially rescued by Scer\GAL4^hs.PH/Atg1^K38Q.UAS

(Scott et al., 2007)

Atg1^Δ3D is partially rescued by Scer\GAL4^hs.PH/Atg1^K38Q.UAS

(Scott et al., 2007)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (11)

Reported As

Symbol Synonym

ATG1^Δ3D

(Bakhoum et al., 2014, Wu et al., 2009)

Atg1^d3D

(Érdi et al., 2012)

Atg1^Δ3D

(Issman-Zecharya and Schuldiner, 2014, Ling et al., 2014, Chang et al., 2013, Shravage et al., 2013, Zirin et al., 2013, Barth et al., 2011, Velichkova et al., 2010, Bass et al., 2009, Chang and Neufeld, 2009, Chang and Neufeld, 2009, Ling et al., 2009, Nezis et al., 2009, Chen et al., 2008, Hou et al., 2008, Juhász et al., 2008, Scott et al., 2007, Scott et al., 2007, Berger et al., 2006)

Atg1^Δ3d

(Braden and Neufeld, 2016, Kim et al., 2013)

Atg1Δ3D

(Tang et al., 2011)

DmATG1^Δ3d

(Lee et al., 2007)

atg1^Δ3D

(Tusco et al., 2017, Rui et al., 2015, Napoletano et al., 2011, Nezis et al., 2010, Nisoli et al., 2010, Shen and Ganetzky, 2009, Nezis et al., 2008)

atg1^Δ3d

(de Castro et al., 2013, Pimenta de Castro et al., 2012)

atg1Δ3D

(Robin et al., 2019, Fouillet et al., 2012)

atg1Δ³

(Melani et al., 2017)

ΔATG1^3d

(Wairkar et al., 2009)

Name Synonyms

Secondary FlyBase IDs

References (40)

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