38A1;39D3-39E1
37F5-38A1;39D3-39E1
37F5-38A1;38B2-38C1
Lar << bk1 << l(2)37Fd << l(2)39ADc << bk2 << Low
Breakpoint(s) molecularly mapped
Does not suppress the ry position effect variegation phenotype associated with In(3R)ryps11136.
Heterozygosity for Df(2L)TW84 results in 3.3% X chromosome nondisjunction and 0.4% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.
Heterozygotes show no adult central brain defect.
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.
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.
Homozygous embryos are very abnormal compared to wild-type.
Heterozygosity for this deletion suppresses the mutant ovarian phenotype of ovoD2.
The Df(2L)TW84 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(2L)TW84 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 one or more nonsuppressing deficiencies.
Ref: Lindsley and Zimm, 1992
Left limit of break 1 from non-inclusion of Lar (FBrf0086508) Right limit of break 1 from inclusion of Lar (FBrf0083926) Limits of break 2 from polytene analysis (FBrf0028752)