The spindle assembly checkpoint (SAC) monitors the metaphase-to-anaphase transition, ensuring correct chromosome segregation in mitosis and meiosis. The SAC assesses the attachment of spindle microtubules to chromosomes via structures called kinetochores; activation of the SAC promotes targeting of securin for degradation by the anaphase-promoting complex/cyclone (APC/C), which in turn promotes chromosome segregation. However, in spermatocytes, meiotic divisions are able to proceed despite the XY sex chromosomes being weakly paired due to poor homology, which should result in SAC silencing. This raises the questions, how does male meiosis proceed and what are the requirements for the SAC? In this study (Chen et al., 2024), Jui-Ching Wu and colleagues investigate the role of the SAC in C. elegans spermatogenesis and find that SAC proteins localize to chromosomes during both meiotic divisions. However, there are differences in the expression of securin, which is present in meiosis I but absent in meiosis II. Interestingly, inhibition of the APC/C or proteasome does not prevent meiosis II from proceeding, suggesting that securin degradation is not the main mechanism regulating meiosis II. Furthermore, perturbation of spindle integrity only triggers a weak SAC response in meiosis I. These findings show that the SAC responds differently in meiosis I and II and provide insights into how spermatocytes have uniquely evolved to evade SAC regulation.
