FB2024_04 , released June 25, 2024
Aberration: Dmel\Df(2L)TE29Aa-11
Open Close
General Information
Symbol
Df(2L)TE29Aa-11
Species
D. melanogaster
Name
FlyBase ID
FBab0001569
Feature type
Also Known As
Df(2L)TE128X11, Df(2L)TE29
Computed Breakpoints include

28E4-28E7;29B2-29C1

Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
Mutagen
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)
Breakpoints
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

l(2)s4199 << bk1 << Btk29A << bk2 << l(2)01482

Genetic mapping information
Comments
Comments on Cytology

All limits from polytene analysis (FBrf0050576)

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

    Inferred to overlap with: Df(2L)BSC111.

    Dominant suppressor of In(1)wm4h position-effect variegation.

    NOT in combination with other aberrations

    One copy of Df(2L)TE29Aa-11 strongly suppresses position effect variegation (PEV) at the w locus caused by In(1)wm4.

    One copy of Df(2L)TE29Aa-11 is unable to suppress the telomeric position effect (TPE) in stocks carrying a variegating P{hsp26-pt-T}39C-5 insertion at the telomere of the left arm of chromosome two.

    The Df(2L)TE29Aa-11 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).

    Little if any macrophage migration occurs in homozygous embryos, with most macrophages remaining in the anterior region, clustered around the foregut, at stage 13-15.

    Fails to complement Df(2L)spd.

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

    Weak second site non-complementing phenotype with zipEbr and zipmhc-c6.1 : malformed phenotype penetrance 10-24%.

    Stocks (2)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (10)
    References (38)