Figure 6.

Schematic depiction of the vertebrate CPC. Different modules potentially execute different functions of the CPC: the activity module (Aurora B in conjunction with the IN-box of INCENP) or the CEN module (the CEN-box of INCENP in conjunction with Borealin and Survivin). Note that Aurora B can indirectly affect CEN module dependent functions due to the role of Aurora B in targeting the CPC to the inner centromere (as depicted by the top part of the cartoon). The dependency of each of the functions on inner centromere localization of the CPC is indicated. (1) Not tested in conditions where the CEN module is present but does not localize to the (inner) centromere (Hengeveld et al., 2017). (2) Not tested in conditions where the CEN module is present but does not localize to the (inner) centromere (Haase et al., 2017). (3) Hengeveld et al. (2017). (4) Forcing Aurora B outwards toward the kinetochore-proximal centromere (by expression of CB-INCENP) does not preclude stable KT-MT attachments in cells depleted of Wapl (to maintain cohesion), suggesting inner centromere localization does not contribute to KT-MT stabilization by spatially separating Aurora B from its kinetochore substrates (Hengeveld et al., 2017). (5) Neither CB-INCENP nor Mis12-INCENP can restore mitotic arrest in paclitaxel in the absence of endogenous INCENP (Wheelock et al., 2017). Moreover, mutation of the BIR-domain of Survivin, that prevents inner centromere localization of the CPC, causes a defect in maintaining a paclitaxel-induced arrest (Lens et al., 2006; Yue et al., 2008). (6) MC silencing is disturbed in cells expressing CB-INCENP, but it is unclear if this is due to the close proximity of the Aurora B to its kinetochore substrates or due to constitutive tethering of Aurora B to the outer centromere in this situation (Hengeveld et al., 2017). (7) Haase et al. (2017).