Defects in meiotic prophase can cause meiotic chromosome missegregation and aneuploid gamete formation. Meiotic checkpoints are activated in germ cells with meiotic defects, and cells with unfixed errors are eliminated by apoptosis. How such a surveillance process is regulated remains elusive. Here, we report that a chromosome-coupled ubiquitin-proteasome pathway (UPP) regulates meiotic checkpoint activation and promotes germ cell apoptosis in C. elegans meiosis-defective mutants. We identified an F-box protein, FBXL-2, that functions as a core component within the pathway. This chromosome-coupled UPP regulates meiotic DSB repair kinetics and chromosome dynamic behaviors in synapsis defective mutants. Disrupted UPP impairs the axial recruitment of the HORMA domain protein HIM-3, which is required for efficient germ cell apoptosis in synapsis defective mutants. Our data suggest that an efficient chromosome-coupled UPP functions as a part of the meiotic surveillance system by enhancing the integrity of the meiotic chromosome axis.

减数分裂前期的缺陷可导致减数分裂染色体错误分离和非整倍体配子形成。减数分裂检查点在具有减数分裂缺陷的生殖细胞中被激活，具有未修复错误的细胞通过凋亡被消除。如何监管这样的监视过程仍然难以捉摸。在这里，我们报道了染色体偶联的泛素蛋白酶体途径（UPP）调节减数分裂检查点激活并促进线虫减数分裂缺陷突变体的生殖细胞凋亡。我们鉴定了一种 F-box 蛋白 FBXL-2，它是该通路中的核心成分。这种染色体偶联的 UPP 调节突触缺陷突变体的减数分裂 DSB 修复动力学和染色体动态行为。破坏的 UPP 会损害 HORMA 结构域蛋白 HIM-3 的轴向募集，而 HIM-3 是突触缺陷突变体中有效的生殖细胞凋亡所必需的。我们的数据表明，高效的染色体偶联 UPP 通过增强减数分裂染色体轴的完整性，作为减数分裂监视系统的一部分发挥作用。