Fig. (2).

Model for the establishment of chromosomal instability through the deregulation of Aurora B activity and cytokinesis failure: both the localization and the kinase activity of Aurora B are promoted by its interaction with cencRNAs. Among other targets, Aurora B phosphorylates CENP-A on its serine 7 residue, and this phosphorylation is necessary for an as-yet unexplained function of CENP-A in cytokinesis. The pharmacological inhibition of Aurora B activity prevents such CENP-A phosphorylation, thereby promoting cytokinesis failure. This defect leads to polyploidy, which in turn promotes the development of multipolar spindles and/or merotelic kinetochore attachments and thus, chromosome mis-segregation. It would be interesting to test whether Aurora B inhibition through depletion of cencRNA has the same effect as its pharmacological inhibition.