Required during anaphase to drive sister chromatid separation to promote flux by actively depolymerizing kinetochore microtubules at their pole-associated minus ends, thereby moving chromatids through a 'poleward flux' (PubMed:14681690, PubMed:20946984, PubMed:24100293). Involved in asymmetric cell division of sensory organ precursor (SOP) cells by playing a role in the asymmetric localization of Sara-expressing endosomes to the pIIa daughter cell but not to the pIIb cell. Klp98A targets Sara-expressing endosomes to the central spindle which is symmetrically arranged in early cell division. During late cytokinesis, central spindle asymmetry is generated by enrichment of Patronin on the pIIb side which protects microtubules from depolymerization by Klp10A while unprotected microtubules on the pIIa side are disassembled by Klp10A, leading to the asymmetric delivery of Sara-expressing endosomes to the pIIa daughter cell (PubMed:26659188). Interacts with Alms1a (via C-terminus). Localizes to mitotic centrosomes, spindle poles and centromeres through metaphase (PubMed:14681690). However, the centromeric localization diminishes markedly at the onset of anaphase, leaving the majority of the protein on the spindle poles (PubMed:14681690). Concentrated around the minus ends focused at the poles (PubMed:14681690, PubMed:24100293). Expressed in male germline stem cells and spermatogonia (at protein level). Marked perturbation of mitotic spindle architecture (PubMed:14681690). RNAi-knockdown in the male germline abolishes the asymmetric enrichment of Alms1a to the mother centrosome (PubMed:32965218). Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Kinesin family. MCAK/KIF2 subfamily.