FB2025_01 , released February 20, 2025
Aberration: Dmel\Df(2R)Kr10
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General Information
Symbol
Df(2R)Kr10
Species
D. melanogaster
Name
Deficiency (2R) Kruppel
FlyBase ID
FBab0001981
Feature type
chromosomal_deletion
Also Known As
Df(2R)SB1, Df(2R)krSB1, SB1
Computed Breakpoints include

60E10;60F5

Features within 60E10--60F5
Genomic Maps
Sequence coordinates
2R:25,052,331..25,061,964 (Df(2R)Kr10:bk1)
(Cook, 2016.2.8)
2R:25,288,936..25,288,936 (Df(2R)Kr10:bk2)
(Cook, 2016.2.8)
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
KrIf-1
(Preiss et al., 1985)
Mutagen
X ray
(Gotwals and Fristrom, 1991, Preiss et al., 1985)
Class of aberration (relative to wild type)
chromosomal_deletion
(FlyBase, 2007)
Class of aberration (relative to progenitor)
chromosomal_deletion
(Duffy et al., 1996, Pauli et al., 1995, Germeraad et al., 1992, Gotwals and Fristrom, 1991, Ludwig et al., 1991, Cote et al., 1987, Preiss et al., 1985)
Breakpoints

60E10;60F5

(Preiss et al., 1985)

60E10-60E11;2Rt

(Cote et al., 1987)

60F1;60F5

(Ludwig et al., 1991)

60E10-60F1;60F5

(Duffy et al., 1996, Gotwals and Fristrom, 1991)

60E10-60E11;60F5

(Pauli et al., 1995, Germeraad et al., 1992)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

gsb-n << bk1 << l(2)10481 << l(2)01848 << bk2

Genetic mapping information
Comments

The 2R:25052331..25061964 release 6 coordinates of the left breakpoint are estimates based on figure 2 of FBrf0046110, which mapped the breakpoint to the region between gsb-n and gsb.

(Cook, 2016.2.8)

The 2R:25288936 release 6 coordinate for the right end of Df(2R)Kr10 corresponds to the right end of the 2R genome assembly, because the tip of 2R has been replaced by bands from another chromosome (FBrf0043323).

(Cook, 2016.2.8)

Breakpoint(s) molecularly mapped

(Bopp et al., 1986)

Deletion for entire cloned Kr region; proximal breakpoint at 0 to +3.5 kb on the molecular map (Cote et al., 1987).

Comments on Cytology

Ref: Preiss et al., 1985, Nature 313: 27--32

(Germeraad et al., 1992)

Deficient region is replaced by chromosome length of unknown origin. gsb-n transcript is strongly affected by the deficiency although the transcribed region as well as 10kb of 5' upstream sequences are left intact.

(Cote et al., 1987)

The deficient chromosome segment is replaced by translocated chromosome bands probably derived from chromosome 4.

(Preiss et al., 1985)

All limits from polytene analysis (FBrf0043323)

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 (18)
Phenotypic Data
In combination with other aberrations

Lethal in combination with Df(2R)gsb.

(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)

Df(2R)Kr10/Df(2R)gsb; P{gsb+} have rescued cuticle phenotype

(Gutjahr et al., 1993)

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

(Wustmann et al., 1989)
NOT in combination with other aberrations

Heterozygosity for Df(2R)Kr10 results in 2.4% X chromosome nondisjunction and 1.0% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

(Harris et al., 2003)

Shows no maternal enhancement of dpphr4.

(Nicholls and Gelbart, 1998)

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

(Duffy et al., 1996)

Deficient embryos show an uninterpretable mutant midgut phenotype.

(Bilder and Scott, 1995)

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

(Pauli et al., 1995)

Embryos display a neuroectodermal phenotype, row 5 neuroblasts (neuroblast NB5-2) are transformed to row 3.

(Skeath et al., 1995)

Homozygous exhibit a gsb- Kr- double mutant phenotype.

(Cote et al., 1987)
Stocks (4)
Notes on Origin
Discoverer
 

Revertant

Balancer / Genotype Variants of the Aberration
 
Separable Components
 
Other Comments
 

The Df(2R)Kr10 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), but this is assumed to be a false positive result (the suppressor may not be within the bounds of the deficient region) because the 2L TAS array on the chromosome is reduced (as assayed by in situ hybridization) and it has previously been shown (FBrf0137248, FBrf0158986) that partial or complete deficiency of the 2L TAS array on the homologue suppresses silencing of brown-red variants of P{3'WP-2,wvar}2Lt.

(Mason et al., 2004)

Second breakpoint not reported. Proximal breakpoint maps to position 0 to +3.5 on the map of the 60E9-F1 interval.

(Cote et al., 1987)

Isolated as a revertant of KrIf-1, with normal eye morphology. The reversion of KrIf-1 is not complete and is strongly dependent on the chromosomal background.

(Preiss et al., 1985)
Synonyms and Secondary IDs (11)
References (47)