Insertion of a 4.5-kb insertion of DNA at coordinate +1.7, judged to be a Doc element on the basis of restriction mapping.
Mutant 3rd instar larval brains have a mitotic phenotype; 42.3% of anaphases are abnormal (showing lagging chromatids, chromatin bridges and nondisjunction) in untreated brains. Colchicine-treated mutant brains show 35.8% premature sister chromatid separation (compared to 0.96% in wild type) and have a mitotic index of 0.71 (compared to 2.44 in wild-type treated brains).
The duration of prometaphase in mutant spermatocytes is similar to that in wild-type spermatocytes. Prometaphase is not prolonged by treatment with taxol in mutant spermatocytes, in contrast to wild type. Chromosomes in mutant spermatocytes are less dynamic during early prometaphase than in wild-type spermatocytes, the rate of poleward chromosome motion is markedly reduced. The rate of anaphase poleward motion is reduced in mutant secondary spermatocytes.
Transmission rate of Dp(1;f)J21A through females to progeny is 28%, mit(1)15 mutation has no effect on transmission.
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 to the total number of mitotic figures in larval brains is similar in wild type.
Zw1016 has abnormal mitotic cell cycle phenotype, non-enhanceable by rodX-5
Zw1016 has abnormal mitotic cell cycle phenotype, non-suppressible by rodX-5
Zw1016 is a non-enhancer of abnormal mitotic cell cycle phenotype of rodX-5
Zw1016 is a non-suppressor of abnormal mitotic cell cycle phenotype of rodX-5
Zw1016 has nuclear chromosome phenotype, non-enhanceable by rodX-5
Zw1016 has mitotic anaphase phenotype, non-enhanceable by rodX-5
Zw1016 has nuclear chromosome phenotype, non-suppressible by rodX-5
Zw1016 has mitotic anaphase phenotype, non-suppressible by rodX-5
Zw1016 is a non-enhancer of nuclear chromosome phenotype of rodX-5
Zw1016 is a non-enhancer of mitotic anaphase phenotype of rodX-5
Zw1016 is a non-suppressor of nuclear chromosome phenotype of rodX-5
Zw1016 is a non-suppressor of mitotic anaphase phenotype of rodX-5
Abnormal anaphases and premature sister chromatid separation occur at the same frequency in mit(1)1516 rodX-5 double mutants as in either single mutant alone. There is no additive effect; the range of defects is quantitatively and qualitatively comparable with that for either single mutant.
Lethal phenotype can be rescued by P element mediated transformation of a wild type mit(1)15 gene copy.
Schalet.