减数分裂是真核生物有性生殖的基础，保证了物种的稳定性和遗传多样性。重组酶RAD51和DMC1是减数分裂所必需的。近几年的研究发现RAD51在减数分裂中只起辅助作用。但是目前尚不清楚RAD51如何发挥辅助作用。SMC5/6复合体在进化上高度保守，其在有丝分裂中的作用较为清楚。拟南芥ASAP1是SMC5/6复合体的一个亚基。通过前期的研究，我们发现突变ASAP1可以抑制rad51突变体完全不育的表型，表明RAD51可能负调控ASAP1。本项目将以rad51 asap1双突变体这一绝佳的遗传材料为基础，综合运用遗传学、细胞生物学和生物化学等手段研究RAD51、ASAP1和DMC1之间的关系，揭示它们在减数分裂中的作用。本项目不仅将揭示RAD51在减数分裂中的真正作用，而且将发现SMC5/6复合体具有调控减数分裂的新功能，具有重要的科学意义。

Meiosis is the basis of sexual reproduction in eukaryotes, ensuring species stability and genetic diversity. The recombinases RAD51 and DMC1 are essential for the meiosis. Recent studies showed that RAD51 only plays a supporting role in meiosis. However, it remains unclear how RAD51 supports meiosis. The SMC5/6 complex is evolutionarily conserved and its functions in mitosis were relatively clear. ASAP1 is a subunit of the SMC5/6 complex in Arabidopsis. Through our initial studies, we found that mutation in ASAP1 could suppress the complete sterility of rad51, indicating that RAD51 negatively regulates ASAP1. In this proposal, based on the unique genetic material rad51 asap1, we will study the relationship between RAD51, ASAP1 and DMC1 and reveal their roles in meiosis using genetics, cell biology, and biochemistry approaches. This study will not only uncover the true function of RAD51 in meiosis, but also reveal a novel function of the SMC5/6 complex in meiosis, which has important scientific significance.