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General Information
Symbol
Df(3L)29A6
Species
D. melanogaster
Name
FlyBase ID
FBab0002286
Feature type
Also Known As
29A6
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
Mutagen
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

Argk << bk1 << bol << l(3)67Ab << bk2 << RpS17

Genetic mapping information
Comments
Comments on Cytology

Left limit of break 1 from polytene analysis (FBrf0065574) Right limit of break 1 from inclusion of Rdl (FBrf0054082) Limits of break 2 from polytene analysis (FBrf0065574)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
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

    Df(3L)29A6/Df(3L)DocA embryos exhibit mild defects in cardioblast specification.

    Df(3L)DocA/Df(3L)29A6 animals show pupal lethality.

    NOT in combination with other aberrations

    Df(3L)29A6/+ males are fertile and have no meiotic defects.

    The Df(3L)29A6 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).

    Shows dominant enhancement of dominant haltere phenotype caused by Ubx195 and Ubx9.22.

    Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.

    No second site non-complementing phenotype with zipEbr and zipmhc-c6.1.

    Shows no maternal enhancement of dpphr4.

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

    Deficient embryos show an uninterpretable mutant midgut phenotype.

    Homozygous embryos are very abnormal compared to wild-type.

    Heterozygosity for this deletion suppresses the mutant ovarian phenotype of ovoD2.

    Reduces the activity of the mitochondrial and cytoplasmic isozyme of Argk.

    Stocks (2)
    Notes on Origin
    Discoverer
     

    isolated as lethal over Df(3L)AC1

    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (5)
    References (62)