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General Information
D. melanogaster
Deficiency (2R) cinnabar
FlyBase ID
Feature type
Computed Breakpoints include


Deleted Segment
Sequence coordinates
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

EcR << bk1 << jing << vimar << bk2

Genetic mapping information
Comments on Cytology

Limits of break 1 from polytene analysis (FBrf0102180) Left limit of break 2 from inclusion of vimar (FBrf0102180) Right limit of break 2 from polytene analysis (FBrf0102180)

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
Phenotypic Data
In combination with other aberrations
NOT in combination with other aberrations

The Df(2R)cn88b 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).

Heterozygosity for Df(2R)cn88b results in 1.1% X chromosome nondisjunction and 0.7% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

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

No second site non-complementing phenotype with zipEbr and zipmhc-c6.1.

Semi-lethality of the vimarB6-2-30 mutation is complemented in combination with Df(2R)cn88b.

Shows no maternal enhancement of dpphr4.

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

Deficient embryos show a mutant midgut phenotype: anterior and posterior constrictions fail to form, though small invaginations are present at the appropriate sites.

Homozygous embryos are very abnormal compared to wild-type.

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

Stocks (2)
Notes on Origin

Recovered as apparent cn double recombinants from test crosses of dysgenic-type males that were heterozygous for a maternally derived dp b cn bw second chromosome and paternally derived autosomes extracted from natural populations and capable of promoting male recombination.

Balancer / Genotype Variants of the Aberration
Separable Components
Other Comments
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Deficiency (2R) cinnabar
Secondary FlyBase IDs
    References (27)