Open Close
General Information
Symbol
Dmel\Atg1UAS.cSa
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct a of Scott
FlyBase ID
FBal0221315
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Atg1, UAS-Atg16B, UAS-Atg16A, ATG1 OE
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of the Atg1 AT02023 cDNA.

Allele components
Product class / Tool use(s)
Encoded product / tool
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 )
Comments on Models/Modifiers Based on Experimental Evidence ( 1 )
 

The amelioration of the phenotype in Npc1aKK101077 expressing flies is observed upon simultaneous co-expression of both Atg1Scer\UAS.cSa and Atg13Scer\UAS.cCa. sf161013

Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expressing Rrp4KK108526 under the control of Scer\GAL4ey.PU occasionally induces irregular eyes.

Under standard nutritional conditions, expression of Atg1UAS.cSa under the control of Scer\GAL4GMR.PU leads to a small and rough eye phenotype in adults and to the induction of autophagosomes (identified as mCherry-Atg8 puncta) in the larval eye disc.

Expressing Atg1UAS.cSa under the control of Scer\GAL4GMR.PU causes a severe rough eye phenotype with patchy red pigmentation.

Scer\GAL4Myo31DF-NP0001-mediated expression of Atg1Scer\UAS.cSa results in more contracted gastric caeca, at an earlier time point, compared to controls. At later time points, once the normal induction of autophagy has initiated, midgut removal occurs normally. Mosaic clones overexpressing Atg1Scer\UAS.cSa in the midgut of feeding larvae show higher levels of autophagy and smaller cell size compared to surrounding wild type cells.

Scer\GAL4Myo31DF-NP0001-mediated expression of Atg1Scer\UAS.cSa results in reduced PI3K signalling in the midgut at -4h relative puparium formation, as assayed by localization of phospho-Akt1.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.Switch.PO (temporally controlled via RU486 feeding) during the first 15 days of adulthood leads to a significant increase in mean lifespan and maximum lifespan; expression during days 27-42 leads to a significant decrease in mean lifespan but not maximum lifespan; expression during the entire adult stage leads to a significant decrease in mean lifespan and maximum lifespan, as compared to controls.

Presynaptic expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav-C155 induces neuromuscular junction overgrowth and an increase in bouton number.

Clonal expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP inhibits cell growth.

Scer\GAL4da.G32 Atg1Scer\UAS.cSa embryos show premature elevated autophagy in the amnioserosa at mid-dorsal closure stage, and increased acridine orange staining throughout stage 16, relative to wild type.

Embryos expressing 2X Atg1Scer\UAS.cSa under the control of Scer\GAL4Orct2-cald-GAL4 and Scer\GAL4Kr.PM show a highly penetrant premature amnioserosa dissociation and dorsal closure defects.

Pan-neuronal expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu induces high levels of autophagy. Under these conditions, bouton number is increased more than two-fold.

Scer\GAL4NP2610-3-1-mediated expression of Atg1Scer\UAS.cSa causes larvae to leave their substrate prematurely and die as late stage larvae or during the first phase of pupation. The airway system of these mutants is heavily disturbed and large regions are filled with liquid, indicative of apoptosis.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4GMR.PF results in partial lethality. Surviving adults have much smaller eyes than normal.

The partial lethality caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4GMR.PF can be partially suppressed by co-expression of Atg1K38Q.Scer\UAS. The reduced eye size caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4GMR.PF is rescued by co-expression of Atg1K38Q.Scer\UAS.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4hs.PH induces autophagy.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4Cg.PA in the fat body induces DNA fragmentation (assayed by TUNEL staining) in 17% of cells.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4hs.PH results in the formation of autophagosomes and autolysosomes throughout fat body cells of fed animals.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in clones in the fat body results in a 94% decrease in average cell size compared to controls, together with a corresponding decrease in nuclear size and DNA content.

Cells expressing Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in clones in the wing disc are eliminated within 36 hours of induction, in contrast to wild-type controls. 22% of cells expressing Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in clones in the wing disc have DNA fragmentation (as shown by TUNEL labeling).

Cells expressing Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in clones in the fat body die by apoptosis. These cells also have reduced or absent filamentous actin staining at the cell periphery and often become fragmented and/or are engulfed by neighboring wild-type cells.

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

Atg1UAS.cSa has eye phenotype, non-enhanceable by maskHMS01045/Scer\GAL4GMR.PU

Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Statement
Reference
Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

The co-expression of Atg1Scer\UAS.cSa suppresses the increased midgut cell size resulting from the adulthood-only expression of Atg9HMS01246 under the control of Scer\GAL4Myo31DF-NP0001.

The pupariation delay and increased pupal size observed in flies expressing Npc1aKK101077 under the Scer\GAL4P0206 driver is rescued by simultaneous co-expression of Atg1Scer\UAS.cSa and Atg13Scer\UAS.cCa.

Expression of Atg1Scer\UAS.cSa driven by Scer\GAL4GMR.PF (to induce autophagy) partially suppresses age-dependent retinal degeneration (loss of rhabdomeres from photoreceptors) and restores mitochondrial morphology in trpP365/+ flies. Pink1B9 suppresses the ability of Scer\GAL4GMR.PF>Atg1Scer\UAS.cSa to suppress age-dependent retinal degeneration (loss of rhabdomeres from photoreceptors) in trpP365/+ flies.

The ability of rictorΔ2 to enhance the abnormal wing posture and mitochondrial aggregation phenotypes seen in flies expressing Pink1dsRNA.Scer\UAS under the control of Scer\GAL4Mhc.PW is blocked by co-expression of Atg1Scer\UAS.cSa.

The ability of trcK122A.Scer\UAS.T:Zzzz\FLAG to enhance the abnormal wing posture and mitochondrial aggregation phenotypes seen in flies expressing Pink1dsRNA.Scer\UAS under the control of Scer\GAL4Mhc.PW is blocked by co-expression of Atg1Scer\UAS.cSa.

Atg1Scer\UAS.cSa-induced synaptic overgrowth is suppressed by coexpression of Rae1Scer\UAS.T:Zzzz\TAP (where both are expressed presynaptically under the control of Scer\GAL4elav-C155).

Expression of Atg1Scer\UAS.cSa in the salivary glands under the control of Scer\GAL4fkh.PH in drprΔ5 mutant animals completely suppresses the persistent salivary gland tissue phenotype.

Clonal expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in a Atg13unspecified background inhibits cell growth.

A wnd1 heterozygous background partially suppresses the high levels of autophagy and bouton number found upon expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu. A wnd1 homozygous background completely suppresses the neuromuscular junction overgrowth phenotype.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4elav.PLu partially suppresses the high levels of autophagy and bouton number found upon expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu.

Co-expression of hiwScer\UAS.fl with Atg1Scer\UAS.cSa, under the control of Scer\GAL4elav.PLu significantly suppresses Atg1Scer\UAS.cSa-mediated neuromuscular junction overgrowth.

Co-expression of nwkScer\UAS.cCa with Atg1Scer\UAS.cSa, under the control of Scer\GAL4elav.PLu fails to suppress Atg1Scer\UAS.cSa-mediated neuromuscular junction overgrowth.

A hiwEMS heterozygous or homozygous background significantly enhances the high levels of autophagy and bouton number found upon expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu.

A Atg18Δ585 heterozygous background significantly suppresses neuromuscular junction overgrowth caused by neuronal expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu. Removal of both copies of Atg18 confers almost complete suppression.

Co-expression of S6kSTDE.Scer\UAS under the control of Scer\GAL4elav.PLu, fails to suppress the neuromuscular junction overgrowth phenotype found upon expression of Atg1Scer\UAS.cSa.

Co-expression of S6kSTDETE.Scer\UAS under the control of Scer\GAL4elav.PLu, fails to suppress the neuromuscular junction overgrowth phenotype found upon expression of Atg1Scer\UAS.cSa.

Co-expression of S6kTE.Scer\UAS under the control of Scer\GAL4elav.PLu, fails to suppress the neuromuscular junction overgrowth phenotype found upon expression of Atg1Scer\UAS.cSa.

Co-expression of S6kKQ.Scer\UAS under the control of Scer\GAL4elav.PLu, fails to suppress the neuromuscular junction overgrowth phenotype found upon expression of Atg1Scer\UAS.cSa.

Co-expression of foxoScer\UAS.cWa.T:Avic\GFP rescues the Atg1Scer\UAS.cSa Scer\GAL4NP2610-3-1 phenotype, rescuing larval lethality almost completely to adulthood, though the larval tracheas show some abnormalities, such as a slight thickening of the epithelium.

The partial lethality and reduced eye size caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4GMR.PF is rescued by co-expression of thScer\UAS.cHa.

The induction of autophagy caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4hs.PH is suppressed by Aut110/Df(3L)Cat.

The induction of cell death caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4Cg.PA in the fat body is suppressed by Aut110/Aut110.

The induction of autophagy caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4hs.PH is significantly suppressed by Atg8aKG07569.

The elimination of cells expressing Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP from the wing disc is significantly reduced in a Atg8aKG07569 background.

The induction of autophagy in the fat body of normally fed animals that is caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4hs.PH is significantly reduced if the animals are also carrying gig109/gig192.

The elimination of cells expressing Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP from the wing disc is delayed by co-expression of RhebAV4.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in TorΔP clones in the fat body results in a further decrease in cells size compared to TorΔP single mutant clones.

Xenogenetic Interactions
Statement
Reference

The premature amnioserosa dissociation and dorsal closure defects seen in 2X Atg1Scer\UAS.cSa Scer\GAL4Orct2-cald-GAL4 Scer\GAL4Kr.PM embryos are completely suppressed by co-expression of BacA\p35Scer\UAS.cHa.

The partial lethality caused by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4GMR.PF is rescued by co-expression of BacA\p35Scer\UAS.cHa.

Co-expression of BacA\p35Scer\UAS.cHa delays the death of cells expressing Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in clones in the wing disc, although these cells are eventually eliminated from the disc.

Complementation and Rescue Data
Partially rescues
Comments

The lethality of Atg1Δ3D homozygotes is partially rescued (to 34% viability) by expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4hs.PH in the absence of heat shock.

Atg1Δ3D homozygous larvae expressing Atg1Scer\UAS.cSa under the control of Scer\GAL4hs.PH in the absence of heat shock show no detectable autophagy when well fed, whereas starvation of these animals induces autophagy, indicating that starvation-induced autophagy is rescued.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Atg1Scer\UAS.cSa
Atg1UAS.cSa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Scott
Secondary FlyBase IDs
    References (40)