在减数分裂时，联会复合体的组装能够促进同源重组和遗传交叉的形成，而同源重组反过来又能对联会复合体的组装与解聚产生影响。然而，这种相互调控的分子机制仍未清楚。本研究以模式生物线虫为研究对象，将对联会复合体的一系列组分进行免疫沉淀和质谱分析，从而系统地发现正常减数分裂条件下的联会复合体结合蛋白及其翻译后修饰。本研究还将同时分析在缺少同源重组的突变体线虫内的联会复合体结合蛋白及修饰，将系统地揭示同源重组对联会复合体组分及修饰的影响。通过采用遗传学、细胞学、基因编辑等手段，本课题将在体内研究与同源重组相关的联会复合体结合蛋白及修饰如何调节减数分裂进程，进一步明确联会复合体组装与同源重组相互调控的分子机制。这些研究对寻找人类不育、流产等生殖问题的根源有着重要的意义。

During meiosis, synaptonemal complex (SC) assembly promotes homologous recombination and crossover formation; the recombination process in turn affects the dynamics of the SC. However, the molecular mechanisms underlying these regulations are not clear. This study will use the model organism C. elegans to address the question. Targeting a group of SC components, immunoprecipitation and mass spectrometry analysis will be performed to systematically identify SC-associated proteins and post-translational modifications (PTMs) under the normal process of meiosis. Moreover, identification of SC-associated proteins and PTMs in a mutant strain where the meiotic recombination is missing will also be performed. This will allow the discovery of effects of meiotic recombination on SC components and PTMs. With tools of genetics, cell biology, and genomic editing etc., the in vivo roles of identified SC-associated proteins and PTMs will be further explored. This study will reveal the molecular mechanisms underlying the regulations between SC assembly and meiotic recombination. This study will also contribute to the understanding of errors that cause infertility and miscarriages in human.