Mitotic error correction and the spindle assembly checkpoint: a tension-filled relationship

The fidelity of mitotic chromosome segregation relies on kinetochores detecting sister chromatid bi-orientation to control error correction (EC) and the spindle assembly checkpoint (SAC). The kinetochore-microtubule attachment state needs to be decoded, the signal processed, and transduced, resulting in either stabilization or destabilization of the attachment. Although many crucial players of this process have been identified, the molecular mechanisms underlying signal integration remain an open question. Focusing on the model system Saccharomyces cerevisiae, we explore the interdependent contributions of the conserved protein kinases Mps1 and Ipl1^{Aurora B}, crucial regulators of mitotic chromosome segregation. We discuss how bi-orientation reorganizes the kinetochore attachment site and we present a perspective on how these structural changes can alter kinase localization and activity.