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.

DCAF-13 is required for growth, development, and fertility.

DCAF13 (DDB1 and CUL4 associated factor 13) is a potential oncogene but little is understood about the developmental roles of this highly conserved gene. We characterized the RNAi phenotypes of , the homolog of DCAF13, and show that compared to age-matched control worms, body length is decreased in (RNAi) larvae, suggesting a role of in larval development. In addition, (RNAi) worms display either a failure or delay in reaching the L4 and adult stages.