66B8-66B9;66C9-66C10
66B8-66B9;66C9-66C10
bk1 << E(dpp)66C << bk2 << RpL14
Fails to complement Df(3L)ZP1.
Df(3L)66C-G28/Df(3L)pbl-X1 lethal (Jeanette Natzle)
Df(3L)66C-G28 embryos show defects in tracheal cell migration.
The Df(3L)66C-G28 chromosome acts as a dominant moderate 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).
Little if any macrophage migration occurs in homozygous embryos, with most macrophages remaining in the anterior region, clustered around the foregut, at stage 13-15.
Heterozygosity for Df(3L)66C-G28 results in a high but variable degree of X chromosome nondisjunction (23.3% and 25.8% in two separate experiments) and fourth chromosome nondisjunction (12.7% and 25.0% in two separate experiments) in In(1)FM7/X ; svspa-pol females. Recombination frequency along the length of the third chromosome does not show significant deviation from normal in females carrying a multiply marked third chromosome and Df(3L)66C-G28.
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.
Midgut development of mutant embryos is wild type.
J. Natzle.
Used in D.melanogaster/D.simulans hybrids to map at least four non-overlapping regions on the D.simulans 3R that have effects on the species difference of cuticular hydrocarbon profile.
All limits from polytene analysis (FBrf0086978)