Figure 11

Alternative models of anaphase Aurora B kinase activation and gradient formation. Diagrams A and B depict models of the anaphase midzone. During anaphase, MKLP2 binds the chromosome passenger complex (CPC) to midzone microtubules. MKLP2 plus-end directed motor activity concentrates the CPC in the central most region of the spindle midzone resulting in Aurora B activation such that peak activity is achieved in the center of the spindle midzone. Contact with midzone microtubules, co-activators such as TD60, and/or trans-autoactivation might contribute to Aurora B activation. (A), upon full activation of Aurora B kinase, the CPC is released either through loss of MKLP2-microtubule interactions, or de-polymerization/severing of central midzone microtubules resulting in dissociation of CPC-MKLP2 complexes. This latter model might explain the curious absence of microtubule-bound Aurora B in the central most region of the spindle midzone (Figure 8b). CPC with fully activated Aurora B kinase then diffuses away from the midzone to activate Aurora B in the soluble pool, encounter inactivating phosphatase activity, or be degraded. Alternatively, as in (B), the soluble cytoplasmic pool of CPC diffuses toward the spindle midzone where it is trans-activated by midzone bound CPC with highly active Aurora B. Cellular phosphatase activity (not shown for simplicity) should play a major role in regulation of the Aurora B activity gradient (see text for additional details).