FB2026_02 , released June 18, 2026
FB2026_02 , released June 18, 2026
Allele: Dmel\Tpisgk-1
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General Information
Symbol
Dmel\Tpisgk-1
Species
D. melanogaster
Name
sugarkill
FlyBase ID
FBal0241671
Feature type
allele
Associated gene
Dmel\Tpi
Associated Insertion(s)
Carried in Construct
Also Known As
TPIsugarkill, TPIsgk
Key Links
Genomic Maps

Allele class

hypomorphic allele - genetic evidence

Mutagen
    Nature of the Allele
    Allele class

    hypomorphic allele - genetic evidence

    (Celotto et al., 2006)
    Mutagen
    Progenitor genotype
    Cytology
    Description

    A missense mutation that affects an amino acid that exists at the dimer interface of the expressed protein.

    (Palladino et al., 2007)

    Amino acid replacement: M80T.

    (Celotto et al., 2006)

    Nucleotide substitution: T?C.

    (Celotto et al., 2006)
    Mutations Mapped to the Genome
    Curation Data
    Type
    Location
    Additional Notes
    References
    point_mutation
    3R:30,133,805..30,133,805 [-]
    Nucleotide change:

    T30133805C

    Reported nucleotide change:

    T?C

    Amino acid change:

    M182T | Tpi-PA; M81T | Tpi-PB; M81T | Tpi-PC

    Reported amino acid change:

    M80T

    (Celotto et al., 2006)
    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 ( 1 )
        Modifiers Based on Experimental Evidence ( 1 )
        Disease
        Interaction
        References
        model of  triosephosphate isomerase deficiency
        is ameliorated by TpiK11M
        (Roland et al., 2013)
        Comments on Models/Modifiers Based on Experimental Evidence ( 1 )
         

        The neurological phenotypes of the Tpisgk-1 allele (which can be used to model triosephosphate isomerase deficiency) are genetically complemented by an allele (TpiK11M) which encodes a catalytically inactive enzyme. This suggests a non-metabolic function for Tpi in D.melanogaster, the loss of which contributes significantly to the neurological defects in the Tpisgk-1 animal model.

        (Roland et al., 2013)
        Disease-implicated variant(s)
         
        Phenotypic Data
        Phenotypic Class
        Phenotype Manifest In
        Detailed Description
        Statement
        Reference

        Ratios of redox molecules are significantly shifted towards the oxidised form in homozygous and Tpisgk-1/Tpisgk-js10 animals compared to controls. This phenotype is age-dependent. Mitochondria in homozygous flies are oxidatively stressed, even at a young age.

        Homozygous flies show a "bang sensitive" phenotype and show paralysis at high temperature. Both phenotypes are significantly worsened by treatment with hydrogen peroxide and is significantly improved by treatment with sub-lethal levels of beta-mercaptoethanol.

        Homozygous flies are hypersensitive to hydrogen-peroxide mediated oxidative stress and resistant to high doses of beta-mercaptoethanol compared to controls.

        (Hrizo et al., 2013)

        Tpisgk-1/TpiWT flies show no sign of paralysis or seizures upon mechanical stress.

        Tpisgk-1 homozygotes and Tpisgk-1/Tpisgk-js10 flies show a delay in recovery after mechanical stress compared to controls, at both 3 and 20 days of age.

        Tpisgk-1 homozygotes and Tpisgk-1/Tpisgk-js10 flies show paralysis upon thermal stress, at both 3 and 20 days of age.

        Tpisgk-1 homozygotes and Tpisgk-1/Tpisgk-js10 flies show significantly reduced median longevity compared to controls.

        (Roland et al., 2013)

        The mechanical stress sensitivity of mutant animals is significantly improved if the animals are treated with MG132 or Geldanamycin.

        (Hrizo and Palladino, 2010)

        Mutants show a bang sensitive phenotype at both room temperature and at 29[o]C, taking longer to recover from mechanical stress than control flies.

        (Seigle et al., 2008)

        Tpisgk1 mutants exhibit severely reduced longevity, progressive locomotor deficiency and neural degeneration.

        (Palladino et al., 2007)

        Tpisgk-1/Tpisgk-js10 flies take longer to regain normal locomotion after mechanical stress than control flies. This stress sensitivity is progressive and increases significantly with the age of the flies at all temperatures examined (room temperature, 25oC and 29oC). Severe stress sensitivity is evident much earlier in flies maintained at 25oC or 29oC compared to those raised at room temperature.

        Lifespan of homozygous and Tpisgk-1/Tpisgk-js10 animals is significantly reduced compared to controls at room temperature, 25oC and 29oC. The decrease in lifespan compared to controls becomes more severe as the temperature at which the flies are raised is increased.

        Young Tpisgk-1/Tpisgk-js10 adults do not show neuropathological defects, however, by their median age, they develop marked neuropathology, showing degeneration in the brain and thoracic ganglion. This degeneration is seen in flies raised at room temperature, 25oC and 29oC.

        Mitochondria in the brain and the indirect flight muscle appear normal in homozygous adults.

        (Celotto et al., 2006)
        External Data
        Interactions
        Show genetic interaction network for Enhancers & Suppressors
        Phenotypic Class
        Enhanced by
        Suppressed by
        Statement
        Reference

        Tpisgk-1 has bang sensitive phenotype, suppressible by Hsp8308445

        (Hrizo and Palladino, 2010)

        Tpisgk-1 has bang sensitive phenotype, suppressible by Hsp83e6A

        (Hrizo and Palladino, 2010)

        Tpisgk-1 has bang sensitive phenotype, suppressible by Scer\GAL4Act5C.Switch.PR/Hsc70-4K71S.UAS

        (Hrizo and Palladino, 2010)

        Tpisgk-1 has short lived phenotype, suppressible by Pros26[+]/ProsĪ²61

        (Seigle et al., 2008)
        Phenotype Manifest In
        Additional Comments
        Genetic Interactions
        Statement
        Reference

        The mechanical stress sensitivity of Tpisgk-1 animals is significantly suppressed if they are also mutant for Hsp8308445 or Hsp83e6A.

        The mechanical stress sensitivity of Tpisgk-1 animals is significantly suppressed if they are also expressing Hsc70-4K71S.Scer\UAS under the control of Scer\GAL4Act5C.Switch.PR (in the presence of Mifepristone).

        The mechanical stress sensitivity of Tpisgk-1 animals is enhanced if they are also expressing Hsc70-4Scer\UAS.cEa under the control of Scer\GAL4Act5C.Switch.PR (in the presence of Mifepristone).

        (Hrizo and Palladino, 2010)

        Pros261/+ can partially suppress the reduced median lifespan of Tpisgk-1 homozygous flies when the double mutants are raised at 29[o]C.

        (Seigle et al., 2008)
        Xenogenetic Interactions
        Statement
        Reference
        Complementation and Rescue Data
        Complements

        Tpisgk-R4

        (Celotto et al., 2006)

        Tpisgk-R3

        (Celotto et al., 2006)

        Tpisgk-R2

        (Celotto et al., 2006)

        Tpisgk-R1

        (Celotto et al., 2006)
        Fails to complement

        Tpisgk-js10

        (Celotto et al., 2006)
        Rescued by

        Tpisgk-1 is rescued by Scer\GAL4Act5C.PI/TpiUAS.cCa

        (Celotto et al., 2006)
        Partially rescued by

        Tpisgk-1 is partially rescued by Scer\GAL4Act5C.PI/TpiUAS.cCa

        (Seigle et al., 2008)

        Tpisgk-1 is partially rescued by Scer\GAL4Act5C.PI/Tpisgk-1.UAS

        (Seigle et al., 2008)
        Not rescued by

        Tpisgk-1 is not rescued by Scer\GAL4Act5C.PI/Tpisgk-1.UAS

        (Celotto et al., 2006)
        Comments

        TpiK11M fully complements the mechanical and thermal stress sensitive phenotypes of Tpisgk-1, at both 3 days and 20 days after eclosion. TpiK11M also complements the reduced longevity phenotype of Tpisgk-1. TpiK11M fails to complement the markedly reduced isomerase activity seen in Tpisgk-1.

        (Roland et al., 2013)
        Images (0)
        Mutant
        Wild-type
        Stocks (0)
        Notes on Origin
        Discoverer
        Comments
        External Crossreferences and Linkouts ( 0 )
        Synonyms and Secondary IDs (10)
        Reported As
        Symbol Synonym
        ND14
        (Celotto et al., 2006)
        ND14ND14
        SGK
        (Hrizo et al., 2013)
        TPIsgk
        (Roland et al., 2016, Seigle et al., 2008)
        TPIsugarkill
        (Hrizo et al., 2013, Roland et al., 2013, Hrizo and Palladino, 2010, Seigle et al., 2008)
        Tpisgk-1
        Tpisgk1
        (Seigle et al., 2008)
        Tpisgk
        (Roland et al., 2013)
        sgk1
        (Celotto et al., 2006)
        Name Synonyms
        sugarkill
        (Seigle et al., 2008)
        Secondary FlyBase IDs
        • FBal0138457
        • FBal0194554
        References (8)