Asymmetric cell division (ACD), a process that generates daughter cells with different cell fates and sizes, is a fundamental mechanism for generating cellular diversity during development. We use Drosophila melanogaster neural stem cells, or neuroblasts, to study ACD. Neuroblasts provide an ideal model for ACD since they are intrinsically polarized and divide with physical as well as molecular asymmetry, resulting in a self-renewed stem cell and a smaller ganglion mother cell (GMC). Kinesins, plus-end-directed motor proteins, have previously been implicated in asymmetric cell division and spindle dynamics. However, the specific kinesins that influence ACD and the mechanism by which they do so remains unknown. Elucidating the function of kinesins in cell division will help establish a more holistic view of cell development. To learn the role that kinesins play in asymmetric cell division, we performed an RNAi knockdown-based live-cell imaging screen of most kinesins in Drosophila. We found that knocking down the Drosophila kinesin genes Klp3A, Klp10A, Klp59C, Klp67A, Klp68D, CG14535, cos, or ncd causes the mitotic spindle to bend during metaphase and anaphase. We hypothesize that this phenotype is due to the spindle being so large that it buckles under the pressure of the cell as it divides. We are currently investigating this hypothesis by imaging knockout mutants to confirm this phenotype and tagging each kinesin with GFP to study how these proteins are localized during typical ACD.