Chromosome axis-associated HORMA domain proteins (HORMADs), e.g., ASY1 in Arabidopsis, are crucial for meiotic recombination. ASY1, as other HORMADs, is assembled on the axis at early meiosis and depleted when homologous chromosomes synapse. Puzzlingly, both processes are catalyzed by AAA+ ATPase PCH2 together with its cofactor COMET. Here, we show that the ASY1 remodeling complex is temporally and spatially differently assembled. While PCH2 and COMET appear to directly interact in the cytoplasm in early meiosis, PCH2 is recruited by the transverse filament protein ZYP1 and brought to the ASY1-bound COMET assuring the timely removal of ASY1 during chromosome synapsis. Since we found that the PCH2 homolog TRIP13 also binds to the ZYP1 homolog SYCP1 in mouse, we postulate that this mechanism is conserved among eukaryotes. Deleting the PCH2 binding site of ZYP1 led to a failure of ASY1 removal. Interestingly, the placement of one obligatory crossover per homologous chromosome pair, compromised by ZYP1 depletion, is largely restored in this engineered zyp1 allele suggesting that crossover assurance is promoted by synapsis. In contrast, the engineered zyp1 allele, similar to the zyp1 null mutant, showed elevated type I crossover numbers indicating that PCH2-mediated eviction of ASY1 from the axis restricts crossover formation.

中文翻译：

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PCH2 和 COMET 向联会复合体的双向募集驱动染色体轴重建，导致交叉限制

染色体轴相关的 HORMA 结构域蛋白 (HORMAD)，例如拟南芥中的 ASY1，对减数分裂重组至关重要。ASY1 与其他 HORMAD 一样，在减数分裂早期组装在轴上，并在同源染色体突触时耗尽。令人费解的是，这两个过程都是由 AAA+ ATPase PCH2 及其辅因子 COMET 催化的。在这里，我们展示了 ASY1 重塑复合体在时间和空间上的组装方式不同。虽然 PCH2 和 COMET 在减数分裂早期似乎直接在细胞质中相互作用，但 PCH2 被横向丝蛋白 ZYP1 募集并被带到与 ASY1 结合的 COMET 上，从而确保在染色体突触期间及时去除 ASY1。由于我们发现 PCH2 同源物 TRIP13 也与小鼠中的 ZYP1 同源物 SYCP1 结合，我们假设这种机制在真核生物中是保守的。删除 ZYP1 的 PCH2 结合位点导致 ASY1 去除失败。有趣的是，每个同源染色体对的一个强制性交叉的位置，受 ZYP1 消耗的影响，在这个工程中得到了很大的恢复。zyp1等位基因表明突触促进了交叉保证。相比之下，与zyp1无效突变体相似的工程化zyp1等位基因显示出升高的 I 型交叉数，表明 PCH2 介导的 ASY1 从轴上的驱逐限制了交叉形成。