Loss of the puromycin-sensitive aminopeptidase, PAM-1, triggers the spindle assembly checkpoint during the first mitotic division in .

Puromycin-sensitive aminopeptidases have long been implicated in cell-cycle regulation, but the mechanism remains unknown. Here we show that mutations in the gene encoding the puromycin-sensitive aminopeptidase, PAM-1 , cause chromosome segregation defects and an elongated mitosis in the one-cell embryo. Depleting a known regulator of the spindle assembly checkpoint (SAC), MDF-2 (MAD2 in humans), restores normal mitotic timing to mutants but exacerbates the chromosome segregation defects.