Stu2 colocalizes with budding yeast kinetochores by interacting with polymerizing microtubule plus ends. Furthermore, it destabilizes these plus ends. It is proposed that Stu2-mediated destabilization contributes indirectly to the “catch-bond” activity of yeast kinetochores.

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Using quantitative cell biological observations and mathematical modeling, it is shown that BubR1 recruitment to the kinetochore via Bub1 promotes mitotic checkpoint complex generation, highlighting BubR1’s dual role of directly strengthening the spindle assembly checkpoint and indirectly silencing it.

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During mitosis, unattached kinetochores in a dividing cell generate the anaphase-inhibitory Mitotic Checkpoint Complex (MCC) to activate the Spindle Assembly Checkpoint (SAC) and delay anaphase onset. To generate MCC, these kinetochores recruit MCC constituent proteins including the protein BubR1. The increased local concentration of BubR1 resulting from this recruitment should enhance MCC generation, but prior studies found this not to be the case. We analyzed the contribution of two BubR1 recruitment pathways to MCC generation in human kinetochores. For these analyses, we isolated a subset of the MCC generation reactions to the cytosol using ectopic SAC activation systems. These analyses and mathematical modeling show that BubR1 binding to the SAC protein Bub1, but not to the 'KI' motifs in the kinetochore protein Knl1, significantly enhances the rate of Bub1-mediated MCC generation in the kinetochore. Our work also suggests that Bub1-BubR1 stoichiometry will strongly influence the dose-response characteristics of SAC signaling.