Meiosis consists of two highly conserved nuclear divisions, which allow eukaryotes to maintain their chromosome number through sexual reproduction. The successful completion of meiosis depends on homologous chromosome pairing. Centromere interactions during early meiotic prophase I facilitate homologous chromosome pairing, but the underlying mechanism is unclear. Here, we performed chromatin immunoprecipitation (ChIP)-mass spectrometry (MS) analysis of maize anthers during early meiotic prophase I using anti-CENH3 (centromeric histone H3) antibodies and determined that the cohesin subunit Structural Maintenance of Chromosome 3 (SMC3) interacts with CENH3 during this period. SMC3 is enriched at centromeres and along chromosome arms in threads from leptotene to pachytene and might promote interactions between homologous centromeres. We observed dysfunctional SMC3 assembly in meiotic-specific maize mutants with defective centromere pairing. In SMC3RNAi meiocytes, centromere pairing defects were observed during early meiotic prophase I, SMC3 was weakly associated with centromeres, and SMC3 did not localize to the chromosome arms. In wildtype mitosis, SMC3 is associated with chromatin and is enriched at centromeres from prophase to anaphase. CRISPR-CAS9-induced Zmsmc3 mutants showed premature loss of sister chromatid cohesion and mis-segregation of chromosomes in mitotic spreads. Our findings suggest that in addition to sister chromatid cohesion, ZmSMC3 participates in meiotic centromere pairing.

减数分裂由两个高度保守的核分裂组成，它们允许真核生物通过有性繁殖维持其染色体数目。减数分裂的成功完成取决于同源染色体配对。减数分裂前期I早期的着丝粒相互作用促进了同源染色体配对，但潜在的机制尚不清楚。在这里，我们使用抗CENH3（着丝粒组蛋白H3）抗体对减数分裂前期I早期玉米花药进行了染色质免疫沉淀（ChIP）-质谱（MS）分析，并确定了3号粘附分子亚基的结构维持（SMC3）与CENH3在此期间。SMC3富集在着丝粒和沿染色体臂的从瘦素到粗线的线程中，并可能促进同源着丝粒之间的相互作用。我们观察到功能异常的SMC3大会在着丝粒配对缺陷的减数分裂特异性玉米突变体中。在SMC3RNAi减数分裂细胞中，在减数分裂前期I早期观察到着丝粒配对缺陷，SMC3与着丝粒弱相关，并且SMC3不在染色体臂上。在野生型有丝分裂中，SMC3与染色质相关，并在着丝粒前期到后期富集。CRISPR-CAS9诱导的Zmsmc3突变体显示姐妹染色单体凝聚力过早丧失以及有丝分裂传播中染色体的错误分离。我们的发现表明，除了姐妹染色单体内聚外，ZmSMC3参与减数分裂着丝粒配对。在早期减数分裂前期I期间观察到着丝粒配对缺陷，SMC3与着丝粒弱相关，并且SMC3不在染色体臂上。在野生型有丝分裂中，SMC3与染色质相关，并在着丝粒前期到后期富集。CRISPR-CAS9诱导的Zmsmc3突变体显示姐妹染色单体凝聚力过早丧失以及有丝分裂传播中染色体的错误分离。我们的发现表明，除了姐妹染色单体内聚外，ZmSMC3参与减数分裂着丝粒配对。在早期减数分裂前期I期间观察到着丝粒配对缺陷，SMC3与着丝粒弱相关，并且SMC3不在染色体臂上。在野生型有丝分裂中，SMC3与染色质相关，并在着丝粒前期到后期富集。CRISPR-CAS9诱导的Zmsmc3突变体显示姐妹染色单体内聚力过早丧失和有丝分裂传播中染色体的错误分离。我们的发现表明，除了姐妹染色单体内聚外，ZmSMC3参与减数分裂着丝粒配对。CRISPR-CAS9诱导的Zmsmc3突变体显示姐妹染色单体凝聚力过早丧失以及有丝分裂传播中染色体的错误分离。我们的发现表明，除了姐妹染色单体内聚外，ZmSMC3参与减数分裂着丝粒配对。CRISPR-CAS9诱导的Zmsmc3突变体显示姐妹染色单体凝聚力过早丧失以及有丝分裂传播中染色体的错误分离。我们的发现表明，除了姐妹染色单体内聚外，ZmSMC3参与减数分裂着丝粒配对。