The maternal contribution present in thr¹ mutants is sufficient for normal initial development until mitosis 15. However, sister chromatid separation during mitosis 15 fails, resulting in a slight delay in exit from mitosis 15. Mitosis 16 exhibits a more extensive delay, with bipolar spindles and normal metaphase plates. However, the majority of epidermal cells in thr¹ mutants embryos have only two and not four centrosomes at the stage of mitosis 16.

The sister chromatids fail to separate at anaphase of mitosis 15 in mutant embryos, and during mitosis 16 chromosomes contain twice the number of chromatid arms.

Homozygous embryos have small unelongated Malpighian tubules.

pim^IL thr¹ double mutants resemble pim^IL or thr^unspecified single mutants. thr¹ fzy³ double mutants block temporarily in cycle 15, but then enter mitosis 16 on schedule. Ventral epidermal cells become permanently blocked in metaphase in mitosis 16, similar to fzy^unspecified single mutants. thr¹ fzy³ pim^IL triple mutants have a similar phenotype to fzy^unspecified single mutants.

Sister chromatid separation in the centromeric region fails.

Homozygous embryos display a nuclear holes phenotype, nuclei drop out of the periphery into the interior during mitotic cycles 11 to 13. Heterozygotes exhibit few nuclei that drop from the periphery but embryos double heterozygous for Res¹ thr¹ have large numbers of dropping nuclei (evidence of a strong synergistic interaction between Res¹ and thr¹).

Completion of mitosis 15 is abnormal, anaphase and telophase figures are not found. CycA and CycB staining reveals chromosome separation (chromosome disjunction) is defective. Entry into the next S phase occurs normally but staining reveals abnormal anaphase and telophase figures. Increase in cell size results from the polyploidisation during the progression through multiple cell cycles lacking chromosome separation and cytokinesis. Despite these abnormalities, major developmental events, such as germband retraction, proceed normally. Cell death occurs at very late stage with a higher frequency in mutants than wild type. The mitotic spindle is not defective in promoting the congression of the mitotic chromosomes into the metaphase plate. Later in mitosis only rudimentary signs of spindle elongation are detected. These irregular extended spindles are not accompanied by separation of the chromosomes. The centriole cycle is not affected.

Mitosis takes place correctly in cycles 1-14. Propidium iodide staining reveals that in mitosis 15 abnormalities become evident as areas of cells delayed in mitosis, that subsequently show disorganised chromatin. Careful analysis of syncitial blastoderm embryos shows that a small percentage of nuclei lose their association with the cortex during cycles 11 to 13 and sink into the interior of the embryo. Analysis with propidium iodide, and immunostaining for microtubules, Cen185, CycA and CycB shows that the order of entry into mitosis of each domain is wild type at cycle 14, and BrdU labelling showed that DNA synthesis immediately after mitosis 14 is normal. In cycle 15 the mitotic domains of thr embryos contain mostly metaphase figures with no anaphase figures that characterize wild type: thr embryos show mitotic domains coalesced into large patches. The thr mutation delays metaphase in terms of chromatid separation, even though, by the criterion of cyclin B degradation, the metaphase to anaphase transition proceeds normally.

strong allele embryonic lethal Larval denticles sparse and arranged in few rows, all pointing posteriorly. Denticles larger than normal. Apparently no mitoses after the first post-blastoderm mitosis, resulting in embryos with fewer and larger cells than normal. TSP 4-9 h. Homozygous lethal in embryo. Loss of maternal function results in an early embryonic phenotype with a failure of chromosome segregation at division 15 (Philp and Glover, 1993).

thr[+]/thr¹ is an enhancer of embryo | embryonic cycle 10 | maternal effect phenotype of CycB^+t10

thr[+]/thr¹ is an enhancer of embryo | embryonic cycle 14 | maternal effect phenotype of CycB^+t10