FB2024_03 , released June 25, 2024
Allele: Dmel\AMPKαD1
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General Information
Symbol
Dmel\AMPKαD1
Species
D. melanogaster
Name
FlyBase ID
FBal0213117
Feature type
allele
Associated gene
Dmel\AMPKα
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
P-element activity
(Lee et al., 2007)
Progenitor genotype
AMPKαG505
(Lee et al., 2007)
Cytology
Description

Imprecise excision of the insertion in SNF1AG505, resulting in a deletion of SNF1A sequences.

(Lee et al., 2007)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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

      Mutants die before the mid-pupal stage.

      Embryos lacking both maternal and zygotic SNF1A+ function (derived from homozygous female germline clones) do not develop into larvae. The mutant embryos have severely deformed cuticle structures and ventral denticle belts are missing. Ultrastructurally, the surface of the embryo is roughened and the columnar structure of the epidermis is disorganised. Some cells contain abnormally enlarged nuclei in these embryos, and approximately 30% of mitotic cells are polyploid.

      Homozygous larvae have a high fraction of mitotic brain neuroblasts that show extreme polyploidy.

      (Lee et al., 2007)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressed by
      Statement
      Reference

      AMPKαD1 has abnormal mitotic cell cycle | larval stage phenotype, suppressible | partially by sqhE20.E21

      (Lee et al., 2007)
      NOT suppressed by
      Statement
      Reference

      AMPKαD1 has abnormal mitotic cell cycle | larval stage phenotype, non-suppressible by Lkb1UAS.cLa/Scer\GAL4hs.PB

      (Lee et al., 2007)
      Phenotype Manifest In
      Suppressed by
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      The cuticle defects seen in mutant embryos derived from SNF1AD1 homozygous female germline clones are partially suppressed by sqhE20.E21; the fraction of embryos that form cuticle is increased from approximately 10% to approximately 30%.

      The fraction of SNF1AD1 mitotic larval brain neuroblasts that show extreme polyploidy is decreased if the larvae are also mutant for sqhE20.E21.

      The fraction of SNF1AD1 mitotic larval brain neuroblasts that show extreme polyploidy is not changed if the larvae are also co-expressing lkb1Scer\UAS.cLa under the control of Scer\GAL4hs.PB.

      (Lee et al., 2007)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      AMPKαD1 is rescued by AMPKαWT.UAS/Scer\GAL4Tub.PU

      (Lee et al., 2007)
      Not rescued by

      AMPKαD1 is not rescued by AMPKαKR.UAS/Scer\GAL4Tub.PU

      (Lee et al., 2007)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      Reported As
      Symbol Synonym
      AMPKD1
      (Lee et al., 2007)
      AMPKαD1
      SNF1AD1
      Name Synonyms
      Secondary FlyBase IDs
        References (1)