Aurora-A kinase is one of the key kinases involved in the regulation of mitotic entry and its progression. During cell division, Aurora-A activity is spatiotemporally controlled to achieve faithful chromosome segregation. Aurora-A localizes to spindle poles where it triggers microtubule nucleation and modulates spindle microtubule dynamics to assemble bipolar spindle and kinetochore-microtubule attachments. At anaphase onset, however, the Aurora-A kinase localizes to the spindle midzone where it regulates the microtubule network for central spindle assembly. In cancers, cells overexpressing Aurora-A kinase often show chromosome segregation errors during cell division leading to binucleated cells, genomic instability and aneuploid progeny. Even today, the precise role of Aurora-A kinase in regulating different mitotic events and how its dysfunction causes cancer progression is poorly understood hitherto.

Using the power of light-induced dimerization (LiD) in human cells expressing exogenous Aurora-A, I induced exogenous Aurora-A recruitment to the spindle poles during different stages of mitosis. This approach enabled me to manipulate the spatiotemporal activity of Aurora-A activity within the mitotic spindle.

Using LiD, I observed that 1) forced recruitment of exogenous Aurora-A to the spindle poles increased Aurora-A activity during prometaphase. 2) Asynchronous cells failed to divide when exogenous Aurora-A was over-recruited to the spindle poles at prometaphase onset. 3) Recruitment of exogenous Aurora-A at the spindle poles increased kinetochore-fibers stability and promoted excessive attachments to kinetochores. 4) Removal of exogenous Aurora-A from the mitotic spindle by forced recruitment to mitochondria decreased kinetochore-fibers stability. 5) Partial inhibition of the mitotic kinase PLK1 partially rescued the increased kinetochore-fiber stability and mitotic failure when Aurora-A was overactive at spindle poles.

These observations indicated that exogenous Aurora-A recruitment at the spindle poles perturbed kinase coordination in the establishment of bipolar spindle assembly. This increased the kinetochore-fibers stability and established excessive erroneous kinetochore-microtubule interactions disrupting cell division progression during anaphase. In conclusion, I propose that under overexpression conditions, exogenous Aurora-A overactivity at the spindle poles, via PLK1 activity, enhances spindle microtubule over-stabilization and prevents the cell from completing the division by rapidly exiting mitosis with double DNA.