42A1-42A19;42E2-42E7
42A1-42A19;42E1-42E7
EcR << bk1 << jing << vimar << bk2
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.
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.
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)