FB2024_03 , released June 25, 2024
Aberration: Dmel\Df(2L)al
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General Information
Symbol
Df(2L)al
Species
D. melanogaster
Name
Deficiency (2L) aristaless
FlyBase ID
FBab0001692
Feature type
Also Known As
Df(2)al
Computed Breakpoints include
Genomic Maps
Sequence coordinates
2L:300,574..303,911 [+] (Df(2L)al:bk1)
2L:300,000..306,000 (Df(2L)al:bk1)
2L:476,220..540,599 (Df(2L)al:bk2)
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

U2af38 << bk1 << fs(2)al << bk2 << lwr

Genetic mapping information
Comments

The 2L:300000..306000 release 6 coordinates of the left breakpoint are estimates based on Figure 2 of FBrf0093782.

The 2L:476220..540599 release 6 coordinates of the right breakpoint are estimates. The left extent corresponds to the left end of ush, which published results say is deleted. The right extent corresponds to the left end of lwr, which published results say is not deleted.

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

Breakpoint 1 was linked to an EcoRI-EcoRI restriction fragment. The position of the restriction fragment on the reference sequence was inferred by a FlyBase curator.

Breakpoint(s) molecularly mapped

Comments on Cytology

The distal breakpoint of Df(2L)al is about 300kb from the telomere.

Pi3K21B probably overlaps the distal breakpoint.

Left breakpoint is just before 21C1-21C2, right breakpoint is just before 21D1-21D2.

Left limit of break 1 from polytene analysis (FBrf0031322) Right limit of break 1 from inclusion of al (FBrf0006343) Left limit of break 2 from polytene analysis (FBrf0047732) Right limit of break 2 from polytene analysis (FBrf0098232)

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(2L)al dominantly enhances the transformation of arista to leg phenotype seen in Df(2R)Dll-MP heterozygotes.

    No effect on In(1)wm4h position-effect variegation.

    Viable in combination with In(2LR)alv.

    Df(2L)al/In(2LR)al8 heterozygotes survive poorly; escapers have reduced aristae, broad thoraces, arched wings, incomplete veins and large eyes (Koroshkina and Golubovsky, 1978).

    NOT in combination with other aberrations

    Flies heterozygous for the deletion show a Minute bristle phenotype.

    The Df(2L)al 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)al results in 2.6% X chromosome nondisjunction and 0.0% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

    Wild-type clones made in the ovaries of a mutant female, are significantly larger than clones of heterozygous mutant cells. This size difference is greater in clones initiated at 48 hours after egg laying (AEL) than 2 hours AEL.

    Homozygous Df(2L)al mutants show an increase in cardial and pericardial cells during embryonic development.

    Df(2L)al in combination with a pair of introgressions from D.simulans spanning 30F1-31E7 to 35D7-36A14 Dsim\Int(2L)S and 21A1 to 22D1--23A2 Dsim\Int(2L)D Dsim\Int(2L)D produces fertile male flies. These flies are female sterile.

    Macrophages in homozygotes remain very small and round with a much lower phagocytic index (PI) for apoptotic corpses than wild type (0.26 compared to 3.96). Heterozygotes show a PI of about 1.5.

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

    Shows no maternal enhancement of dpphr4.

    Does not act as a dominant suppressor of Nnd-1.

    Strong enhancer of B.

    Midgut development of mutant embryos is wild type.

    Maternal hemizygosity for Df(2L)al significantly increases post-fertilization embryonic mortality. Paternal hemizygosity has no effect.

    Homozygous embryos do not complete head involution and tracheae are disconnected.

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

    Heterozygotes have an extreme Minute phenotype with rough eyes.

    Homozygous lethal heterozygous Minute phenotype

    Stocks (4)
    Notes on Origin
    Discoverer

    E.B. Lewis, 1940.

     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (7)
    References (82)