FB2025_01 , released February 20, 2025
Aberration: Dmel\Df(2L)Gpdh1-A
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General Information
Symbol
Df(2L)Gpdh1-A
Species
D. melanogaster
Name
FlyBase ID
FBab0001468
Feature type
Also Known As
Df(2L)GdhA, Df(2L)GpdHA, Df(2L)gdh-A
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

cype << bk1 << l(2)25Ea << l(2)26Ad << bk2 << l(2)26Cf

Genetic mapping information
Comments

Breakpoint(s) molecularly mapped

Comments on Cytology

H2.0 maps (by in situ hybridisation) to the right of the Df(2L)GpdhA deficiency.

Limits of break 1 from polytene analysis (FBrf0048198) Left limit of break 2 from inclusion of lid (FBrf0067338) Right limit of break 2 from polytene analysis (FBrf0041503)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Partially deleted / disrupted
Molecular Data
Partially deleted
Genes NOT Deleted / Disrupted
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
 
Molecular Data
 
Affected Genes Inferred by Location (0)
    If no genes are listed here, it may be because the affected region is very large. The JBrowse insert above may show an error for the same reason, and other FlyBase tools such as CytoSearch may also fail for large regions. You can contact FlyBase for more help.
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    Phenotypic Data
    In combination with other aberrations

    Df(2L)x528/Df(2L)Gpdh1-A is embryonic lethal and impacts founder cells for lateral transverse muscle 3, lateral transverse muscle 4, lateral oblique muscle 1 and ventral transverse muscle 1; loss of lateral transverse muscles.

    Df(2L)x528/Df(2L)Gpdh1-A embryos show a loss of neuroblasts NB1-1, NB2-5 and NB2-4. This loss is much more pronounced in odd-numbered than even-numbered abdominal segments. However, the loss is similar to mid mutants, suggesting that the it is deletion of the mid gene and not the H15 gene that is causing the phenotype.

    Inferred to overlap with: Df(2L)x528.

    Df(2L)Gpdh1-A/Df(2L)x528 larvae show a loss of denticle belts; denticle rows 1 to 5 are frequently lost in odd-numbered segments, whereas even-numbered segments show milder defects. Df(2L)H15-x4/Df(2L)Gpdh1-A larvae show a weak loss of denticles phenotype.

    Enhances position effect variegation at the w locus caused by In(1)wm4, C(1;YL)wmMc or T(1;4)wm5 and position effect variegation at the y locus caused by In(1)y3P.

    Lethal in combination with Df(2L)cl7. Lethal in combination with Df(2L)Gpdh1-78. Lethal in combination with Df(2L)Gpdh1-75. Lethal in combination with Df(2L)cl1. Lethal in combination with Df(2L)cl2.

    NOT in combination with other aberrations

    Heterozygosity for Df(2L)Gpdh1-A results in 8.0% X chromosome nondisjunction and 2.2% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

    Shows no maternal enhancement of dpphr4.

    Dominantly causes tergite defects in less than 50% of run3 heterozygotes.

    Midgut development of mutant embryos is wild type.

    Homozygous embryos are very abnormal compared to wild-type. The hindgut is short and broad, and the Malpighian tubules do not elongate.

    Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.

    Enhance mottling in wm4.

    Stocks (2)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (15)
    References (62)