Pleuger et al. investigate the regulation of Mps1 association with the kinetochore receptor Ndc80 complex during mitotic checkpoint signaling. They find that a conserved N-terminal segment of Mps1 binds to the neck region of Ndc80:Nuf2, located at the backside of the paired CH domains. Point mutations in this interface impair SAC signaling and cause growth defects. The same interface binds the Dam1 complex, which is crucial for kinetochore end-on attachments. The error correction kinase Ipl1 controls the competition between Dam1 and Mps1 for the binding site on Ndc80c. Ipl1 phosphorylation of the Dam1 C terminus prevents Dam1 from displacing Mps1 during anaphase onset, allowing sustained SAC signaling. The study reveals a novel mechanism where Mps1 is recruited to kinetochores and released upon bi-oriented kinetochore-microtubule attachments, highlighting the integration of the error correction process with mitotic checkpoint signaling.Pleuger et al. investigate the regulation of Mps1 association with the kinetochore receptor Ndc80 complex during mitotic checkpoint signaling. They find that a conserved N-terminal segment of Mps1 binds to the neck region of Ndc80:Nuf2, located at the backside of the paired CH domains. Point mutations in this interface impair SAC signaling and cause growth defects. The same interface binds the Dam1 complex, which is crucial for kinetochore end-on attachments. The error correction kinase Ipl1 controls the competition between Dam1 and Mps1 for the binding site on Ndc80c. Ipl1 phosphorylation of the Dam1 C terminus prevents Dam1 from displacing Mps1 during anaphase onset, allowing sustained SAC signaling. The study reveals a novel mechanism where Mps1 is recruited to kinetochores and released upon bi-oriented kinetochore-microtubule attachments, highlighting the integration of the error correction process with mitotic checkpoint signaling.