The COMA/CENP-H/I kinetochore complex regulates microtubule dynamics at kinetochores. The complex is also required to generate spindle checkpoint signals in both yeast and human cells under conditions where Aurora B activity is compromised. Our data explain why mammalian cells treated with Aurora inhibitors still have a functional spindle assembly checkpoint (SAC), since the checkpoint signals through CENP-H/I/N. The SAC effect from depleting the CENP-H/I/N complex cannot be explained by a weakened SAC signal, and the complex has no role in the SAC response to paclitaxel. We propose a model to explain the differential response of human cells to nocodazole and paclitaxel.

The N-terminal tail of Ndc80 is essential for kinetochore-microtubule binding in human cells but is not required for viability in yeast. We show that the yeast Ndc80 tail is required for timely mitotic progression and accurate chromosome segregation. The tail is essential when cells are limited for Dam1, demonstrating a redundant function for the Ndc80 and Dam1 complexes in vivo.