The spindle assembly checkpoint (SAC) prevents the onset of anaphase in the presence of unattached kinetochores. Human kinetochores, however, have multiple microtubule-attachment sites, and it has so far remained elusive how the SAC responds to partial kinetochore occupancy. Now, Geert Kops and co-workers (Etemad et al., 2019) assay SAC silencing in instances of submaximal microtubule–kinetochore binding. By analysing the association of SAC components with kinetochores at varying levels of microtubule occupancy, the authors find that the MAD1, MAD2 and RZZS components of the checkpoint are removed even at low microtubule occupancy, whereas the BUB1 and BUBR1 components typically remain associated even at higher occupancy levels. Indeed, inhibition of the SAC kinase MPS1 causes loss of BUB1, but not MAD1, from kinetochores, suggesting that the kinetochore removal from the MAD1–MAD2–RZZS and BUB1–BUBR1 modules is governed by distinct mechanisms. Moreover, by using phosphomimetic HEC1 mutants, in which the capacity of kinetochores to capture microtubules is reduced, they demonstrate that MAD2 is removed from kinetochores even under conditions of intermediate microtubule binding. Overall, these results show that SAC silencing occurs even at submaximal kinetochore–microtubule engagement, with different mechanisms governing the silencing of the MAD1–MAD2–RZZS and BUB1–BUBR1 components.

• © 2019. Published by The Company of Biologists Ltd