Xu Jing, Zhou Lian, Chen Kaixin, Huang Runsen, Niu Baixiao, Ye Juanying, Ma Hong, Copenhaver Gregory P, Wang Yingxiang
Guangdong Basic Research Center of Excellence for Precise Breeding of Future Crops, Guangdong Laboratory for Lingnan Modern Agriculture, Guangdong Provincial Key Laboratory for the Development Biology and Environmental Adaptation of Agricultural Organisms, College of Life Sciences, South China Agricultural University, Guangzhou 510642, China.
School of Biology and Agriculture, Shaoguan University, Shaoguan 512005, China.
Plant Cell. 2025 Jun 4;37(6). doi: 10.1093/plcell/koaf089.
Faithful chromosome segregation is essential for both mitotic and meiotic cell division. The anaphase-promoting complex/cyclosome (APC/C) and its coactivators are required for meiotic chromosome segregation, but their potential targets and regulatory mechanisms remain unclear in plants. Here, we performed a ubiquitinome analysis and show that Arabidopsis thaliana Aurora 1 (AUR1) is over-ubiquitinated at lysine 102 in the coactivator Cell Division Cycle 20.1 (cdc20.1) mutants and that AUR1 overexpression can partially rescue the cdc20.1 meiotic defect. We also demonstrate that APC/C ubiquitinates AUR1, leading to its degradation through the 26S proteasome pathway. Moreover, the APC/C subunit and coactivators Cell Cycle Switch 52 A2/B (CCS52A2/B) and CDC20.1 interact with AUR1 both in vitro and in vivo. Intriguingly, CCS52A2/B promotes AUR1 ubiquitination and degradation, while CDC20.1 prevents AUR1 degradation. Consistent with this finding, AUR1 levels are lower in cdc20.1 and higher in ccs52 mutants relative to Col-0, and mutation of CCS52A2/B causes defects in meiotic spindle assembly and homologous chromosome segregation. Genetic analyses demonstrate that Arabidopsis anaphase-promoting complex/cyclosome subunit 8 (APC8), CDC20.1, CCS52 and AUR1 act in the same pathway to control meiotic spindle assembly and homologous chromosome segregation. Thus, this work provides mechanistic insight into the role of APC/C coactivators in regulating AUR1 homeostasis during meiosis in plants.
准确的染色体分离对于有丝分裂和减数分裂细胞分裂都至关重要。后期促进复合物/细胞周期体（APC/C）及其共激活因子是减数分裂染色体分离所必需的，但它们在植物中的潜在靶标和调控机制仍不清楚。在这里，我们进行了泛素组分析，结果表明，在共激活因子细胞分裂周期20.1（cdc20.1）突变体中，拟南芥极光激酶1（AUR1）在赖氨酸102处过度泛素化，并且AUR1的过表达可以部分挽救cdc20.1的减数分裂缺陷。我们还证明，APC/C使AUR1泛素化，导致其通过26S蛋白酶体途径降解。此外，APC/C亚基和共激活因子细胞周期开关52 A2/B（CCS52A2/B）和CDC20.1在体外和体内均与AUR1相互作用。有趣的是，CCS52A2/B促进AUR1的泛素化和降解，而CDC20.1则阻止AUR1的降解。与这一发现一致，相对于Col-0，cdc20.1中AUR1的水平较低，而在CCS52突变体中较高，并且CCS52A2/B的突变会导致减数分裂纺锤体组装和同源染色体分离缺陷。遗传分析表明，拟南芥后期促进复合物/细胞周期体亚基8（APC8）、CDC20.1、CCS52和AUR1在同一途径中发挥作用，以控制减数分裂纺锤体组装和同源染色体分离。因此，这项工作为APC/C共激活因子在植物减数分裂过程中调节AUR1稳态的作用提供了机制上深入的了解。
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