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. 2010 Nov 15;191(4):795–808. doi: 10.1083/jcb.201006028

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© 2010 Woodruff et al.

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Figure 8. — Multiple pathways regulating distinct subprocesses drive spindle disassembly. (A) Summary of phenotypic analysis for nine spindle disassembly mutants. Decreased half-spindle shrinkage rate indicates that the mean rate of half-spindle shrinkage was significantly lower than the wild-type rate (P < 0.05; Table I). Additionally, elevated half-spindle recovery rate indicates that the spindle-half recovery frequency was >1.5-fold higher than the wild-type frequency. (B) Multiple pathways model for spindle disassembly. In the first pathway (blue box), the APC loaded with the late anaphase cofactor Cdh1 (APC^Cdh1) degrades cross-linking MAPs (e.g., Ase1, Cin8, and others) to facilitate separation and destabilization of spindle halves. In the second pathway (red box), Aurora B (Ipl1 in yeast) phosphorylates the spindle stabilizer EB1 (Bim1 in yeast) and the spindle destabilizer She1. The ARF-C complex is needed for EB1 phosphorylation by Aurora B. The COMA kinetochore complex loads She1 onto the spindles. In the third pathway (green box), the kinesin-8 family member Kip3 actively depolymerizes spindle MTs and prevents their regrowth during mitotic exit. Inhibition of multiple pathways produces additive defects on spindle-half disassembly and cell fitness.