Deletion of 90 amino acids (158-247), removing the H1 heptad repeat.
dorsal appendage (with Df(2L)TW119), with BicDr5
egg, with Df(2L)TW119/BicDr5
egg (with Df(2L)TW119), with BicDr5
egg chorion, with BicDH2
egg chorion, with BicDH3
egg chorion (with Df(2L)TW119), with BicDr5
microtubule organizing center & oocyte
Mutant ovaries contain mostly mutant egg chambers containing no oocyte, and very rarely an egg chamber chamber producing an abnormal egg (2 or 3 per ovary). The number of germ-cells in mutant egg chambers is variable. In BicDH mutants the differentiation of the follicle cells is not affected, but the migration of the cells can be abnormal. During stage 2b Fas3 expressing follicle cells migrate between the interconnected cystocytes of the germline cysts, rather than migrating only on the surface of the cysts. Second, gaps in the follicle cell layer are occasionally detected in region 3 of the germarium. In BicDH mutants bipolar egg chambers are sometimes seen. Defects in the nuclear morphology of oocyte nuclei are seen, Occasionally polyploidy and intermediate polyploidy is seen in the oocyte nucleus of these egg chambers. The formation of the microtubule organising centre (MTOC) seen in germarial region 2a is normal. However the polarised microtubule network starts to break down at subsequent stages in most egg chambers.
The occasional egg produced by BicDH1, BicDr5/Df(2L)TW119 females shows a strongly ventralised chorion phenotype and does not develop. BicDH1 enhances the phenotype of BicDH2 and BicDH3, i.e. fewer eggs are laid than for BicDH2 or BicDH3 alone and more of the laid eggs are more severely ventralised.
Rescues zygotic viability of BicDr5/Df(2L)TW119 at rates ranging from 85% to 95%. Cannot rescue the female sterility defect of BicDr5/Df(2L)TW119.