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

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 C. elegans 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 pam-1 mutants but exacerbates the chromosome segregation defects. Thus, PAM-1 is required for proper attachment of chromosomes to the mitotic spindle and its absence triggers the SAC.

DCAF-13 is required for C. elegans 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 dcaf-13 , the C. elegans homolog of DCAF13, and show that compared to age-matched control worms, body length is decreased in dcaf-13 (RNAi) C. elegans larvae, suggesting a role of dcaf-13 in larval development. In addition, dcaf-13 (RNAi) worms display either a failure or delay in reaching the L4 and adult stages. Our data also indicates that dcaf-13 (RNAi) treatment beginning at L4 stage does not increase embryonic lethality in progeny; however, progeny production was significantly decreased in dcaf-13 (RNAi) worms, suggesting a general role in fertility and perhaps oocyte development.