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

## TL;DR

This study shows that a protein called PAM-1 is important for proper cell division in C. elegans embryos, and its absence activates a checkpoint that prevents errors in chromosome separation.

## Contribution

The study reveals a novel role for PAM-1 in triggering the spindle assembly checkpoint during early cell division in C. elegans.

## Key findings

- Loss of PAM-1 causes chromosome segregation defects and prolonged mitosis in C. elegans embryos.
- Depletion of MDF-2 (a SAC regulator) restores mitotic timing but worsens chromosome segregation issues in PAM-1 mutants.
- PAM-1 is essential for proper chromosome-spindle attachment and its absence activates the SAC.

## Abstract

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.