INCENP acts like a rheostat to adjust levels of aurora B activity and determine CPC behavior. (A) Status of the CPC, levels of aurora B (AurB) activity (shown as a degree of red shading), and localization of the complex during metaphase and anaphase in cells expressing the different INCENP mutants. Levels of aurora B activity are based on those measured in Fig. 5 B. (B) Nonenzymatic subunits of CPC regulate aurora B localization and activity. An INCENP–Borealin (Bor)–Survivin (Svn) subcomplex is sufficient for centromere targeting and is required for the stability of the individual components. The INCENP C terminus acts as a rheostat, controlling the level of aurora B kinase activity. (C) Functional consequences of the differing levels of aurora B kinase activity set by interactions with the INCENP C terminus. If aurora B is inhibited with ZM447439, the kinase is inactive, and the spindle checkpoint response to low dose taxol is defective. In INCENP^OFF cells and INCENP^OFF cells expressing INCENP^W766G, aurora B activity is ∼15–20% higher, but the spindle checkpoint response to low dose taxol remains defective. In INCENP^OFF cells expressing INCENP^F802A, aurora B activity is a further ∼10% higher. These cells now exhibit a normal checkpoint response to low dose taxol. In all of these cells, aurora B activity is insufficient to promote CPC transfer from centromeres to the anaphase spindle midzone.