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. 2015 Oct 2;5(1-2):1–12. doi: 10.1080/19490992.2015.1090669

Figure 2.

Figure 2.

Spindle assembly checkpoint (SAC) inactivation in response to kinetochore microtubule attachment. In the presence of kinetochore microtubules attached end-on (to both Knl1 and Ndc80), Aurora B activates Plk1, which triggers PP2A binding to BUBR1 on phosphorylated KARD motif and causes the dephosphorylation of the RVSF/SILK motifs, thereby alleviating the inhibition of PP1 binding on to the Knl1. The binding of PP1 dephosphorylates the MELT repeats and the SAC components are released from the KMN network, extinguishing the SAC to an “off” state. Cdk1 also phosphorylates BUBR1 and augments PP2A binding to BUBR1. Further, in the presence of microtubules, Mps1 can no longer bind to Ndc80 and the phosphoswitch-mediated signaling subsides. For details on the amino acid map of all the Knl1 motifs, please refer to Fig. 1 legend.