Faithful chromosome segregation during mitosis is essential for the generation of a viable cell progeny, with an identical set of chromosomes at each cell division. Inaccuracies in chromosome segregation lead to abnormalities in chromosome number, known as aneuploidy, a major cause of spontaneous miscarriages and birth defects, and a hallmark of human cancers. In eukaryotic cells a highly conserved surveillance system, the spindle assembly checkpoint (SAC), operates during mitosis to delay mitotic progression under conditions that could compromise accurate chromosome segregation. During mitosis, spindle checkpoint components are recruited to unattached kinetochores and produce an inhibitory signal that blocks the E3 ubiquitin ligase, APC/C. When all kinetochores acquire stable bipolar attachments, the checkpoint is quickly and irreversibly switched off, leading to APC/C activation and ubiquitination of several mitotic substrates, allowing anaphase onset and mitotic progression. Our team is interested in better understaning the mechanisms underlying mitotic progression and its regulation by the spindle assembly checkpoint and to evaluate the plasticity of those processes and how they can be modified to adapt to the different requirements associated with eukaryotic diversity.