FB2025_01 , released February 20, 2025
Aberration: Dmel\Df(3R)tll-g
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General Information
Symbol
Df(3R)tll-g
Species
D. melanogaster
Name
Deficiency (3R) tailless
FlyBase ID
FBab0002940
Feature type
Also Known As
Df(3R)tllg, Df(3R)tllG
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

Dlw << bk1 << spdo << dco << bk2 << bnk

Genetic mapping information
Comments

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

Comments on Cytology

Limits of break 1 from polytene analysis (FBrf0079523) Limits of break 2 from polytene analysis (FBrf0064685)

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 (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
    NOT in combination with other aberrations

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

    Does not give a Minute phenotype when heterozygous.

    The Df(3R)tll-g chromosome does not act as a dominant 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).

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

    Mutant embryos fail to develop normal stomodeal nervous system ganglia, though remnants can be observed.

    Homozygous embryos do not complete tracheal formation. The hindgut is very short or absent, the Malpighian tubules are absent, the posterior midgut primordium is reduced and midgut fusion is variable.

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

    The Bolwig organ is often enlarged, and the stomatogastric nervous system is abnormal in homozygous embryos. The frontal ganglion and frontal commissure are shifted anteriorly and the recurrent and frontal nerves are not fully developed. The labral nerve projects anteriorly. The optic lobes are reduced in size.

    Heterozygotes with Dlw1 are viable and have the Dlw1/Dlw+ phenotype, transformation of ventral into dorsal wing compartment.

    In srp,tll double mutants neither a duplicated hindgut structure (as in srp embryos) nor a hindgut as in hkb,srp embryos develops, although the posterior midgut primordium invaginates.

    Lack hindgut, Malpighian tubules and much of the posterior midgut.

    Individuals have an abnormal dorsal cephalopharyngeal apparatus.

    Stocks (2)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (6)
    References (37)