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General Information
D. melanogaster
Deficiency (2R) Kruppel
FlyBase ID
Feature type
Also Known As
Df(2R)SB1, Df(2R)krSB1, SB1
Computed Breakpoints include
Sequence coordinates
2R:25,052,331..25,061,964 (Df(2R)Kr10:bk1)
2R:25,288,936..25,288,936 (Df(2R)Kr10:bk2)
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

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

Genetic mapping information

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.

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for the right end of Df(2R)Kr10 corresponds to the right end of the 2R genome assembly, because the tip of 2R has been replaced by bands from another chromosome (FBrf0043323).

Breakpoint(s) molecularly mapped

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

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.

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

All limits from polytene analysis (FBrf0043323)

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

Lethal in combination with Df(2R)gsb.

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.

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

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

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.

Shows no maternal enhancement of dpphr4.

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

Deficient embryos show an uninterpretable mutant midgut phenotype.

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

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

Homozygous exhibit a gsb- Kr- double mutant phenotype.

Stocks (4)
Notes on Origin


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.

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

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.

Synonyms and Secondary IDs (11)
References (43)