FB2024_03 , released June 25, 2024
Aberration: Dmel\Df(2L)30A-C
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General Information
Symbol
Df(2L)30A-C
Species
D. melanogaster
Name
FlyBase ID
FBab0001390
Feature type
Also Known As
Df(2L)30C, Df(2L)30A;C
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

raw << bk1 << Cks30A << l(2)DA2 << bk2 << ms(2)30C

Genetic mapping information
Comments

This deletion removes a single ribosomal protein-coding gene (though other genes are also removed).

Comments on Cytology

Ref: Lindsley and Zimm, 1992

Left limit of break 1 from polytene analysis (FBrf0058516) Right limit of break 1 from inclusion of tai (FBrf0067338) Left limit of break 2 from polytene analysis (FBrf0093373) Right limit of break 2 from polytene analysis (FBrf0080145)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Partially deleted / disrupted
Molecular Data
Completely deleted
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
    Phenotypic Data
    In combination with other aberrations
    NOT in combination with other aberrations

    Flies heterozygous for the deletion do not show a Minute bristle phenotype.

    The Df(2L)30A-C chromosome acts as a dominant weak suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{wvar}KR3-2", a stable "brown-red" variant of the P{3'WP-2,wvar}2Lt insertion).

    Heterozygosity for Df(2L)30A-C results in 2.1% X chromosome nondisjunction and 2.5% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

    83% of hemisegments show an RP2 to RP2sib cell fate transformation in homozygous embryos.

    Intermediate second site non-complementing phenotype with zipEbr and zipmhc-c6.1 : malformed phenotype penetrance 25-75%.

    Shows no maternal enhancement of dpphr4.

    Shows a dose-sensitive interaction with pbhs.PB.

    Deficient embryos show a mutant midgut phenotype: midgut primordia do not migrate from terminalia.

    Midgut primordia do not fuse, but remain at the anterior and posterior of the yolk mass in homozygous embryos. The hindgut is somewhat shorter than normal. The Malpighian tubules bud out but do not elongate.

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

    Stocks (2)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (8)
    References (46)