FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\AMPKα3
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General Information
Symbol
Dmel\AMPKα3
Species
D. melanogaster
Name
FlyBase ID
FBal0241421
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
AMPK3
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

16bp deletion (nucleotides 422-437 relative to the translation start site of NM_057965.4). This results in amino acid Tyr141 being converted to a stop codon.

16bp deletion creating a stop codon at residue 141.

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

A 16 bp deletion (attgccaccggcacat) in AMPKalpha resulting in a stop codon at Y141.

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

Hemizygous AMPKα3 males do not survive to adulthood.

AMPKα3 follicle cell clones show normal polarity under both well-fed and starvation conditions. Polarity is also maintained after feeding flies drugs that reduce cellular ATP levels and activate AMPK, though many egg chambers degenerate at stage 7/8.

Cells within AMPKα1 follicle clones are larger than adjacent wild type cells, under both fed and starved conditions.

Homozygous mutants display a completely penetrant phenotype of significantly enlarged plasma membrane domains in dendrites but not in axonal compartments of da neurons in second instar larvae.

Mutant embryos have a normal somatic muscle pattern. The number of nuclei in the segmental border muscle is normal.

Heterozygous flies are more resistant to P. entomophila infection than control flies.

SNF1A3 mutants exhibit aberrant morphology in class IV multi-dendritic neurons.

SNF1A3 mutants die as larvae and are characteristically smaller than wild-type larvae of the same age.

The majority of SNF1A3 mutants die between the fifth and seventh day of the third instar larval stage. Feeding these larvae with Rapamycin increases the percentage of mutant larvae surviving to the seventh day.

Under fed conditions, SNF1A3 larvae show significantly more and larger lipid droplets in oenocytes compared to controls, resembling the starved phenotype of wild-type oenocytes.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The pupal-stage lethality of hemizygous AMPKα3 males can be partially rescued by expression of S6kKQ.Scer\UAS under the control of Scer\GAL4tub.PU but not by expression of either of the following: TorTED.Scer\UAS, TrpmlScer\UAS.cVa, SNF4AγScer\UAS.T:Avic\GFP.

The pupal-stage lethality of hemizygous AMPKα3 males can be partially rescued by combination with either Trpml1 or Trpml2.

The pupal-stage lethality of hemizygous AMPKα3 males can be partially rescued by expression of TrpmlJF01239 RNAi under the control of Scer\GAL4Act.PU.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

The pupal stage lethality observed in either AMPKα1 or AMPKα3 hemizygous males can be partially rescued by expression of AMPKαScer\UAS.cMa under the control of Scer\GAL4tub.PU.

Scer\GAL4Ubi-mediated expression of SNF1AScer\UAS.T:Disc\RFP-mCherry rescues viability and fertility in SNF1A3 mutants.

Scer\GAL4Ubi-mediated expression of SNF1AScer\UAS.cMa rescues viability in SNF1A3 mutants.

Scer\GAL4109(2)80-mediated expression of SNF1AScer\UAS.cMa rescues the dendritic phenotype of SNF1A3 mutants.

Expression of SNF1AScer\UAS.cMa under the control of Scer\GAL4109(2)80 rescues the neuronal defects of SNF1A3 mutants.

Expression of SNF1AΔC.Scer\UAS under the control of Scer\GAL4109(2)80 fails to rescue the neuronal defects of SNF1A3 mutants.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (11)