Klp67A^322b24/Df(3L)29A6 flies are male sterile and female semi-sterile.

Klp67A^322b24/Df(3L)29A6 mutant syncytial embryos display premature mitotic spindle elongation.

Klp67A^{Ubi-p63E.T:Avic\GFP} restores fertility and viability to Klp67A^322b24/Df(3L)29A6 mutants. The major mitotic defect caused by depletion of Klp67A in the mutant embryos is rescued by Klp67A^{Ubi-p63E.T:Avic\GFP}. Klp67A^{Ubi-p63E.T:Avic\GFP} restores wild-type spindle morphology and geometry and the dynamics of mitotic spindle poles in the rescued flies is virtually identical to that seen in wild-type embryos.

Klp67A^322b24/Df(3L)29A6 mutant spermatocytes show defects throughout meiosis. In late prophase I, and to a lesser extent in late prophase II, asters ectopically localize close together in the cytoplasm, instead of at opposite sides of the nucleus. Despite this defect, the majority of primary spermatocytes assemble a bipolar spindle, form a metaphase plate and proceed through anaphase. The spindles of anaphase and metaphase I and II have astral microtubules that are longer than wild type and show abnormal chromosome segregation. In telophase I and II the astral microtubules are even longer and the central spindle is often absent or much less dense than in wild type. A minority of spermatocytes in anaphase I and II have two nuclei of different sizes. Almost half of the cells in ana-telophase II contain two spindles within the same cytoplasm, suggesting cytokinesis failure during the first meiotic division. These cells also have long astral microtubules that overlap, causing highly disorganized spindle architecture. Spermatocytes in telophase I with a normal central spindle display a regular contractile ring; those with a poorly organized central spindle appear unable to assemble a contractile ring. Klp67A^322b24/Df(3L)29A6 mutant spermatids often have an unusually large nebenkern associated with two or four nuclei, consistent with a failure in meiotic cytokinesis. Additionally, some spermatids contain nuclei of irregular sizes, consistent with defects in chromosome segregation during meiosis. Some mutants have polyploid spermatocytes with four not two centrosomes, suggesting that Klp67A is involved with cytokinesis in the gonial mitoses that precede meiotic division. Blastoderm embryos from Klp67A^322b24/Df(3L)29A6 mothers show abnormal spindle formation and architecture throughout mitosis. During prophase, most centrosomes do not complete migration to opposite sides of the nucleus and the period from centrosome migration to nuclear breakdown is longer than in wild-type embryos. The incomplete centrosome separation causes spindles to become distorted and banana-shaped to accommodate extended microtubules from spindle poles. In some metaphase spindles, centrosomes detach from the spindle poles. Additionally, the metaphase spindle is increased in length, whether centrosome separation is normal or not. The interval between nuclear envelope breakdown and the appearance of a central spindle is longer than wild type due to an increase in time spent in metaphase and anaphase B. Unlike in wild type, mutant spindles continue to increase in length during metaphase and pole separation occurs later in anaphase B. During telophase, most spindles are missing a normal central spindle or have a greatly reduced number of midzone microtubules, which are not organized in the typical dense lateral array seen in wild type. Following telophase, two daughter spindles can form during ensuing divisions. Despite the above defects, chromosome segregation appears to proceed as in wild type.