FB2024_03 , released June 25, 2024
Aberration: Dmel\Df(2R)gsb
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General Information
Symbol
Df(2R)gsb
Species
D. melanogaster
Name
FlyBase ID
FBab0001966
Feature type
chromosomal_deletion
Also Known As
Df(2R)IIX62, Df(2R)gsbIIX62
Computed Breakpoints include

60E9;60F1

Features within 60E9--60F1
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
Mutagen
ethyl methanesulfonate
(Gotwals and Fristrom, 1991)
Class of aberration (relative to wild type)
chromosomal_deletion
(FlyBase, 2007)
Class of aberration (relative to progenitor)
chromosomal_deletion
(Germeraad et al., 1992, Cote et al., 1987)
Breakpoints

60E9;60F1

(Cote et al., 1987)

60E9-60E10;60F1-60F2

(Germeraad et al., 1992)
Causes alleles
zipIIX62
(Blake et al., 1998, Young et al., 1993)
gsbIIX62
Carries alleles
Transposon Insertions
Formalized genetic data

bk1 hits zip << Tkr << bk2 << Kr

Genetic mapping information
Comments

Deficiency breakpoint within the zip locus.

(Young et al., 1993)

Proximal breakpoint at -55 to -49 kb and distal breakpoint at +40 to +42.5 kb (Cote et al., 1987), with the proximal breakpoint of Df(2R)SB1 approximately at 0.

Comments on Cytology

Ref: Nusslein-Volhard et al., 1984, Roux Arch. dev. Biol. 193: 267--282

(Germeraad et al., 1992)

Left limit of break 1 from polytene analysis (FBrf0046110) Right limit of break 1 from inclusion of zip (FBrf0045941) Left limit of break 2 from inclusion of Tkr (FBrf0046110) Right limit of break 2 from polytene analysis (FBrf0046110)

Sequence Crossreferences
DDBJ / EMBL / GenBank
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

    Lethal in combination with Df(2R)Kr10.

    (Kahsai et al., 2016)

    Ecol\lacZY72 staining of Df(2R)gsb/Df(2R)Kr10 mutants suggests aCC and pCC neurons are not duplicated (contrary to results of FBrf0049834). Df(2R)gsb/Df(2R)Kr10 mutants exhibit duplicated RP2 neurons and lack U and CQ neurons, phenotype can be rescued by gsb+t20.1 (though rescue of U and CQ neurons is incomplete). Posterior commissures are missing or reduced, phenotype varies between segments but no segment is wild type.

    (Duman-Scheel et al., 1997)

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

    (Wustmann et al., 1989)

    Df(2R)gsb/Df(2R)SB1 embryos express gsb but not zip (Cote et al., 1987).

    NOT in combination with other aberrations

    Heterozygous embryos do not show defects in the SNa axons.

    Homozygous embryos show replacement of the posterior part of each segment with a mirror-image duplication of denticle belts normally found in the anterior part of each segment.

    (He and Noll, 2013)

    In the embryonic motor system of mutant animals exhibit frequently fused ISN and SN nerve roots but the respective dendritic fields do not appear to intermingle.

    (Landgraf et al., 2003)

    Mutant embryos show an increase in apoptotic nuclei in the anterior portion of the segment similar to that seen in wgl-12 and arm8, though the increase in cell death is restricted to the ventral and ventrolateral surface of the embryo. There is also a slight in crease in cell death in the ventral en-expressing cells.

    (Pazdera et al., 1998)

    Neuroblast NB5-2 is transformed into MP2.

    (Bhat and Schedl, 1997)

    Homozygotes exhibit duplication of the RP2 lineage due to NB5-3 changing to NB4-2 identity. Simultaneous elimination of gsb rescues the RP2 lineage in 70% of ptcH84 hemisegments. Ectopic expression of P{HS-wg} causes triplication of the RP2 lineage.

    (Bhat, 1996)

    Cuticular phenotype is rescued by the construct P{gsb-prd}.

    (Li and Noll, 1994)

    Defective in gonad assembly.

    (Warrior, 1994)

    P{gsb+} rescues the cuticle phenotype of Df(2R)gsb homozygotes or heterozygotes with Df(2R)Kr10.

    (Gutjahr et al., 1993)
    Stocks (2)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     

    The Df(2R)gsb chromosome may 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), but the eye colour phenotype in the presence of Df(2R)gsb overlaps the eye colour phenotype in a wild-type background so it cannot be unequivocally demonstrated that the deficiency chromosome uncovers a suppressor of telomeric silencing. In addition, any suppression is a false positive result (the suppressor is not within the bounds of the deficient region) because the region of the deficiency is covered by a combination of nonsuppressing deficiencies and deficiencies with suppressors that map to the 2L tip.

    (Mason et al., 2004)

    Df(2R)ES1/Df(2R)gsb embryos fail to complete dorsal closure.

    (Young et al., 1993)

    Distal breakpoint maps to position +40 to +42.5 and the proximal breakpoint to position -55 to -49 on the map of the 60E9-F1 interval.

    (Cote et al., 1987)
    Synonyms and Secondary IDs (9)
    References (47)