cnn^HK21 homozygous pupae have a failure to prune all ddaC dendrites by 16 h after puparium formation (APF), unlike controls.

cnn^HK21 homozygous third instar larval brains display a significant decrease in volume, as compared to controls.

Apparently normal ciliary rootlets form in the olfactory neurons of cnn^HK21/cnn^25cn1 adults.

cnn^HK21/Df(2R)cnn embryos have a persistent meiotic-like spindle when development is detectable. A variety of spindle shapes located at the cortex is detected in 34% of the mutant embryos and often observed only a few nuclei deep in the cytoplasm of the embryo. Approximately 7% of the mutant embryos display multiple nuclei at the cortex, but lack deep divisions and an obvious remnant of the meiotic spindle. The final class of mutant embryos that develop (32%) have a mix of cortical and deep divisions and a persistent large spindle associated with the cortex. All other embryos examined (27%) either lack any detectable signs of development or are necrotic. Polar body formation is never observed in the mutants in either haploid/diploid or a triploid configuration.

cnn^ΔEx1A embryos in a cnn^HK21/Df(2R)cnn mutant background fail to cellularize.

The most common nuclear type in prophase stage embryos expressing any one of cnn^{S22A.PA.Scer\UAS.P\T.T:Avic\EGFP}, cnn^{S22A.T27A.PA.Scer\UAS.P\T.T:Avic\EGFP} or cnn^{T27A.PA.Scer\UAS.P\T.T:Avic\EGFP} under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} in a cnn^HK21/Df(2R)cnn mutant genetic background appears to be haploid with most nuclei located at the cortex, but deep divisions are still observed in less than 5% of animals. Polar body formation or persistent meiotic-like spindle is not detected in the mutant embryos. Development fails well before cellularization in the transgenic animals.

During the early larval stage, cnn^HK21 mutants show no defects in photoreceptor differentiation or pattern formation. However, from the mid-pupal (50%) developmental stage, the cnn^HK21 mutation causes acetylated microtubule bundle mispositioning and apical domain localisation defects.

Only 37% of testis somatic cyst stem cells show repositioning of the mitotic spindle during anaphase in cnn^mfs3/cnn^HK21 males compared to 78% of cases in heterozygous controls.

Mutant embryos have a reduced number of pole cells compared to controls and the pole cells that do form often have greatly reduced germ plasm.

In mutant spermatids, the proximal centriole-like structure forms, though the gamma-tubulin collars of the centrioles are largely reduced and almost absent or show an abnormal localization.

cnn^HK21 mutants have an increased number of brain neuroblasts, and 12-13% of the metaphase neuroblasts show aberrant spindle orientation orthogonal to the apical/basal cortical polarity axis. This subset of neuroblasts showing aberrant spindle orientation always generate equal-sized siblings that both assume neuroblast identity.

Single cnn^HK21 neuroblast clones often give rise to two or more neuroblast sibling cells, but never two basal ganglion mother cells.

Embryogenesis fails during the first few cleavage divisions in mutant animals, and most embryos examined show no signs of development.

cnn^HK21 embryos exhibit a 'linked spindles' phenotype, indicative of defective cleavage furrows.

Third-instar larval neuroblasts from cnn^HK21 mutants exhibit mitotic spindles with broad poles, lacking astral microtubules.

One copy of cnn^HK21 is unable to suppress position effect variegation (PEV) at the w locus caused by In(1)w^m4.

One copy of cnn^HK21 is unable to suppress the telomeric position effect (TPE) in stocks carrying a variegating P{hsp26-pt-T}39C-5 insertion at the telomere of the left arm of chromosome two.

Anaphase onset is considerably delayed in cnn^HK21 mutants.

cnn^HK21 mutants normally suffer little aneuploidy (~1%) and survive to adulthood.

In embryos laid by cnn^HK21 homozygous females, the centrioles are associated with appreciable amounts of PCM, but are often not properly centered within it. The centrioles appear to be constantly nucleating PCM but seem unable to maintain their connection to it. The centrioles often exhibit irregular, stochastic movements, leaving a trail of PCM behind them as they move away. As a result of this behavior, the centrioles in cnn^HK21 embryos often lose their attachment to the nuclear envelope in interphase and to the spindle poles in mitosis. The centrosomes in cnn^HK21 embryos organise astral microtubule arrays but seem unable to maintain their connection with them. when the embryos enter mitosis, many nuclei are not associated with centrioles, and anastral spindles assemble around the mitotic chromatin. Many nuclei, however, are close enough to a centriole for the astral microtubules to contribute to spindle assembly. However, these centrioles fail to maintain their position at the spindle pole and either wander around within the spindle or lose their connection to the spindle altogether. The dramatic mitotic defects in cnn^HK21 mutant embryos results from the failure of the centrioles to maintain a stable connection to the PCM and microtubules that they organise.

In most cnn^HK21 neuroblasts, no prominent MTOC is detectable before nuclear envelope breakdown, and spindle assembly occurs largely by an acentrosomal pathway. Nonetheless, approximately 95 of cnn^HK21 neuroblasts ultimately divide asymmetrically, whereas approximately 4% divide symmetrically and 1% fail in cytokinesis. Although this failure rate is modest, it is still significantly higher than in wild-type.

For homozygous mutant male germline stem cells where one of the two centrosomes is positioned next to the hub, it is essentially random whether the mother or daughter centrosome stays next to the hub (in contrast to wild type where the daughter centrosome migrates away from the hub).

In mutant males, mitotic spindles are not oriented towards the hub in about 30% of dividing germline stem cells (GSCs) examined (in contrast to wild-type males where the mitotic spindles of the GSCs are always oriented perpendicular to the hub-GSC interface). In an additional 10-20% of mutant GSCs, the spindles are properly oriented, but the proximal spindle pole is no longer closely associated with the cell cortex at the hub-GSC interface and the entire spindle is displaced away from the hub. The frequency of spindle orientation defects is highest in metaphase. Interphase centrosome positioning is partially randomised in the mutant GSCs; in more than 35% of mutant GSCs with duplicated centrosomes, neither centrosome is positioned next to the hub (in wild-type male GSCs with duplicated centrosomes, one centrosome remains adjacent to the hub). Dividing GSCs with misoriented or detached spindles, which lose attachment to the hub are seen. Hub size is not significantly different in mutant males compared to wild type. The number of germ cells associated with the hub is increased 20-30% in homozygous males, from an average of 8.94 GSCs per hub in wild type to 11.89 GSCs per hub in homozygotes. In mutant testes with many stem cells, GSCs appear crowded around the hub and often seem attached to the hub by only a small region of cell cortex. The number of germ cells associated with the hub is increased 20-30% in homozygous males, from an average of 8.94 GSCs per hub in wild type to 10.69 GSCs per hub in cnn^HK21/cnn^mfs3 males. In some cases in cnn^HK21/cnn^mfs3 testes, a GSC divides and the two daughter cells remain in contact with the hub (this is not observed in the wild type).

Adult lies have black dots on their wings. Mitotic figures from mutant larval brains have no (cnn staining) centrosomes at the spindle poles. Mutant spindles appear meiotic in character, with the smaller forth chromosomes migrating to the spindle poles precociously. Despite the absence of mitotic centrosome centrioles with normal morphology can be found. The spindle microtubules appear to assemble outward from the chromosomes. Astral microtubules are absent at prophase. cnn^HK21 neuroblasts are found to be oriented improperly approximately 22% of the time.

Homozygous females produce embryos that arrest prior to cellularisation. Embryos derived from cnn^HK21/Df(2R)cnn females have severe defects in nuclear division and distribution. The embryos never achieve cellularisation.

cnn^HK21 embryos show a lack of spindle pole localisation of centrosome associated antigens Cp190 and γTub23C in a variable manner, suggesting that the Microtubule Organising Centres are at least structurally and functionally impaired, or possibly missing altogether. Embryos from cnn^E2/cnn^HK21 mothers exhibit an abnormal and disorganised spatial arrangement of nuclei during syncitial divisions, becoming increasingly severe during later divisions. This leads to a cessation of development before formation of a cellular blastoderm. In contrast to wild-type, embryos from cnn^HK21 mothers show an unstructured cortical microfilament organisation during syncitial development. Syncitial embryos from cnn^E2/cnn^HK21 mothers, show abnormally shaped mitotic spindles that are characteristically squat with ill-defined poles. During interphase and prophase, a variable number (as opposed to strictly two in wild type) of spread out and less discrete astral microtubule-like structures are seen, despite having no γTub23C localising nucleating core.

Eggs derived from homozygous females initiate development and cytoplasmic clearing occurs in a narrow zone around the egg periphery (in wild-type embryos this process is coupled to the arrival of the nuclei at the periphery). The eggs do not seem to develop beyond this stage; pole cells are not formed and cellularisation does not occur. However, about two hours after cytoplasmic clearing, the egg periphery starts to show local contractions, in what might be an attempt at gastrulation. These contractions eventually lead to eggs which typically have one or two condensed yolk balls surrounded by more transparent cytoplasm.

maternal-effect lethal Homozygous females lay eggs in which a narrow halo of clear cytoplasm appears around the time when nuclei would be expected to migrate to the egg periphery, but no cellularization takes place. female-sterile

cnn[+]/cnn^HK21 is an enhancer of partially lethal - majority die | maternal effect phenotype of Df(2L)Fs(2)Ket-RX32/Cen^f04787

cnn^HK21 is an enhancer of abnormal mitotic cell cycle phenotype of mad2^G6595

cnn^HK21 is an enhancer of abnormal mitotic cell cycle phenotype of msd1^ex51

cnn^HK21, mad2^G6595 has abnormal neuroanatomy | third instar larval stage phenotype

cnn^HK21, mad2^G6595 has abnormal size | third instar larval stage phenotype

BubR1^KEN.mRFP1, cnn^HK21 has lethal | pupal stage phenotype

BubR1^KEN.mRFP1, cnn^HK21 has abnormal mitotic cell cycle phenotype

cnn^HK21, msd1^ex51 has lethal phenotype

cnn^HK21, mad2^G6595 has lethal phenotype

cnn^HK21, mad2^G6595 has abnormal mitotic cell cycle phenotype

cnn^HK21, mad2^G6595 has abnormal cell cycle phenotype