Motor proteins contact microtubules and chromosomes to create moving forces. One main force acts on attached kinetochores, but kinesins also exert forces on chromosome arms for chromosome congression and alignment, generating a polar ejection force (PEF). The chromokinesin Kid has been shown to control PEF, which needs to be reduced or abolished following anaphase onset to enable a change of chromosome directionality from anti-poleward to poleward movement. In Xenopus egg extracts, Kid is degraded to allow for poleward chromosome movements. In mammalian cells, however, this is not the case and they must, therefore, regulate Kid differently to reduce PEF. On page 3609, Miho Ohsugi and colleagues report that the phosphorylation state of the Kid amino acid residue Thr463 controls a PEF-ON or PEF-OFF state for chromosome movement in mouse embryonic fibroblasts and oocytes. The authors show that dephosphorylation of Thr463 reduces PEF. Moreover, Kid's second microtubule-binding domain (MTBD) and a coiled-coil domain are required for the suspension of PEF. In Kid−/− oocytes – in which Kid activity is dispensable for metaphase chromosome alignment – expression of a phosphomimetic form of Kid, or deletion of the second MTBD or the coiled-coil domain causes partially segregated chromosomes to move back to the metaphase plate. This work proposes a model in which a Kid-activity switch mediates the state of the PEF to allow chromosome segregation in anaphase.
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