The mitotic index of mutant larval brains is 0.96, compared to 1.02 in wild-type brains. Mutant brains incubated with colchicine do not show an increase in mitotic index, even after 1 hour of drug treatment, in contrast to wild-type brains, which show a doubling of the mitotic index in this time. Mutant larval brain neuroblasts treated with colchicine often do not arrest in prometaphase (which occurs in wild-type neuroblasts in response to colchicine), but instead enter an anaphase-like state with separated sister chromatids.
Adult escaper males are sterile, testes are small and contain immotile sperm. Mutant onion stage spermatids vary considerably in size, indicative of chromosome missegregation during both meiotic divisions (nondisjunction during anaphase). Mistakes in chromosome behaviour are visualised by lagging chromosomes and chromatin bridges. Meiotic as well as mitotic defects are specific for events occurring either at anaphase onset or during anaphase proper. Mutation does not cause precocious sister chromatid separation (PSCS) during the first meiotic division but does affect cytokinesis (spermatids containing more than one nucleus per nebenkern).
Embryos derived from homozygous germline clones generally terminate development in the late syncytial blastoderm stages, although 15-25% of develop to later stages of embryogenesis, and 1% hatch into larvae. Mitotic synchrony is lost in embryos derived from homozygous germline clones. Chromatin bridges between nuclei, unequal segregation of chromosomes and lagging chromatids are seen at anaphase.
Brain cells are hyperploid. Aneuploidy involves improper chromosome segregation at anaphase: precocious sister chromatid separation. Mitotic index and the ratio of numbers of cells in anaphase relative to the total number of mitotic figures in larval brains is similar in wild type.
Zw1017 is a suppressor of abnormal mitotic cell cycle phenotype of aspE3
Lethal phenotype can be rescued by P element mediated transformation of a wild type mit(1)15 gene copy.
