asp^L1/asp^E3 transheterozygous adults exhibit a smaller brain, due to smaller central brain and optic lobe, as compared to controls.

All homozygous pharates present a striking reduction of the head size while abdomen and thorax seem unaffected. Transheterozygous combinations with asp¹, asp^L1, asp^MB11367 or Df(3R)BSC519 show a similar phenotype. At third instar larval stage, asp^E3 brains are significantly smaller, particularly the optic lobes, compared to wild type.

At third instar larval stage, asp^E3 brains show a severely reduced population of optic lobe neuroblasts. Lamina neurons are absent and the the volume occupied by neuroepithelial cells in the optic lobe is reduced. However, there are no defects in neuronal populations derived from other regions of the brain and all cell populations are present (even if reduced in size).

At late third instar larval stage, asp^E3 brains exhibit striking defects in the organization and shape of the neuroepithelium.

Even if mitotic spindles are partly unfocused in asp^E3 neuroepithelial cells, they assemble in bipolar fashion and do not arrest at pro metaphase or show cytokinesis defects. However, errors in chromosome segregation occurs in ~23% of mutant neuroepithelial cells.

At third instar larval stage, asp^E3 brains show increased apoptosis. Whereas in wild type optic lobes the number of apoptotic cells decreases at mid and late L3, the number of such cells increase in asp^E3 brains - all apoptotic cells seem to be neuroepithelial.

At third instar larval stage, the cells of asp^E3 mutant neuroepithelium show a premature switch in spindle position (from parallel to perpendicular to the plane of the epithelium). This defect doesn't impact cell fate determination.

In contrast to wild type, dividing nuclei of the asp^E3 neuroepithelium are broadly distributed along the apical-basal axis, with nuclei positioned either too apical or too basal. Mutants also show an increase in interphase cell height and nuclear density. However, centrosomes are positioned normally in mutant interphase cells.

The initial velocity of separation between cell junctions after laser ablation is higher in asp^E3 neuroepithelial cells compared to wild type, suggesting an increase in apical cell junction tension at the level of the adherens junctions in the mutant. Accordingly, the apical surface area of asp^E3 neuroepithelial cells is reduced compared to wild type.

asp^{ΔC.Ubi.T:Avic\GFP} asp^E3 have normal head size but flies die soon after hatching.

asp^{ΔN.Ubi.T:Avic\GFP} asp^E3 animals show severe defects in neuroepithelial morphology, develop slowly and die before pupation.

Unlike wild-type, asp^E3/asp^L1 mutant spermatocytes at late prophase are still located at the plasma membrane, where they remain throughout meiosis. The microtubule organising centres (MTOCs) are found at the periphery of mutant spermatocytes, unlike in controls where the MTOCs are seen near the nuclear membrane. Microtubule organisation is significantly different to wild-type in mutant spermatocytes. At the time of nuclear envelope breakdown (NEB), a distinct focus of microtubule polymerisation appears within the nuclear region, away from the asters. It gives rise to a few bundles that grow and get organised into a bipolar spindle-shaped microtubule array that in 28% of cells is anastral and establishes no contact with the membrane-bound centrosomes. The remainder are accounted for by cell in which, despite the distance, microtubules from one or both asters reach the spindle so that spindle poles and asters are aligned. The timing of meiosis progression from nuclear envelope breakdown (NEB) to anaphase onset seems to be largely unaffected. Chromosome segregation is abnormal in these cells. During prometaphase, the bivalents do not move to the extent that they do in control cells. Congression occurs, but orientation is rarely bipolar. Homologue chromosomes separate at the onset of anaphase, but they barely move, remaining near the centre of the spindle. Moreover they tend to cosegregate and end up included in the same daughter nucleus. Cytokinesis does proceed to completion in around half of mutant cells. These cells contain unconnected centrosomal asters and anastral spindles. These anastral spindles can be observed at any angle, even 90^oC with respect to the position of the two asters. In most such cases, furrow progression forces the spindle to rotate and align with asters so that at the end, a fairly normal cytokinesis takes place. The orientation of the plane of cleavage keeps a tight 90+-10^o with respect to the axis defined by the asters and does not correlate with the orientation of the anastral spindle.

Nearly all mitotic cells in mutant larval brains arrest in prometaphase with highly condensed chromosomes, resulting in a greatly increased mitotic index (9.05, compared to 1.02 in wild-type brains).

The frequency of mitotic figures in the asp^E3 larval brain is higher than in wild-type. 25% of mitotic figures are polyploid. Anaphase and circular mitotic figures are extremely rare.

The size and the frequency of the cuticular clones are higher than in control flies. There is a correlation between the amount of maternally contributed asp product and the frequency and size of asp clones. Maternally derived products are sufficient to carry out normal cell division until late in development (stage unspecified).

Unfertilized eggs have either no nuclei or a small number of large nuclei, free centrosomes and independent arrays of microtubules. Fertilized eggs from homozygous asp mutant females have this phenotype and embryos that undergo varying degrees of aberrant morphogenesis. The embryos have free centrosomes, abnormal arrays of microtubules and have large areas that are devoid of or have a reduced number of nuclei. Brain neuroblasts of homozygous asp larvae have a high mitotic index and have condensed chromosomes as if blocked at metaphase. Immunostaining reveals that many cells have a single centrosome connected to the metaphase chromosomes by microtubules connected in a hemi-spindle-like structure.

asp^E3 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by sqh^{A20.A21.Tag:FLAG}

asp^E3 has increased cell death | third instar larval stage phenotype, suppressible by Scer\GAL4^C855a/BacA\p35^UAS.cHa

asp^E3 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^C855a/BacA\p35^UAS.cHa

asp^E3 has abnormal mitotic cell cycle phenotype, suppressible by BubR1^KEN.mRFP1

asp^E3 has abnormal mitotic cell cycle | larval stage phenotype, suppressible by mad2^Δ

asp^E3 has abnormal mitotic cell cycle phenotype, suppressible by BubR1^k03113

asp^E3 has abnormal mitotic cell cycle phenotype, suppressible by Zw10¹⁷

asp^E3 has abnormal mitotic cell cycle phenotype, suppressible by rod^X-5

asp^E3 has embryonic/larval brain | third instar larval stage phenotype, suppressible by sqh^{A20.A21.Tag:FLAG}

asp^E3 has embryonic/larval brain | third instar larval stage phenotype, suppressible by Scer\GAL4^C855a/BacA\p35^UAS.cHa