Meiotic crossovers (COs) are important for reshuffling genetic information between homologous chromosomes and they are essential for their correct segregation. COs are unevenly distributed along chromosomes and the underlying mechanisms controlling CO localization are not well understood. We previously showed that meiotic COs are mis-localized in the absence of AXR1, an enzyme involved in the neddylation/rubylation protein modification pathway in Arabidopsis thaliana. Here, we report that in axr1^-/-, male meiocytes show a strong defect in chromosome pairing whereas the formation of the telomere bouquet is not affected. COs are also redistributed towards subtelomeric chromosomal ends where they frequently form clusters, in contrast to large central regions depleted in recombination. The CO suppressed regions correlate with DNA hypermethylation of transposable elements (TEs) in the CHH context in axr1^-/- meiocytes. Through examining somatic methylomes, we found axr1^-/- affects DNA methylation in a plant, causing hypermethylation in all sequence contexts (CG, CHG and CHH) in TEs. Impairment of the main pathways involved in DNA methylation is epistatic over axr1^-/- for DNA methylation in somatic cells but does not restore regular chromosome segregation during meiosis. Collectively, our findings reveal that the neddylation pathway not only regulates hormonal perception and CO distribution but is also, directly or indirectly, a major limiting pathway of TE DNA methylation in somatic cells.

减数分裂交换（COs）对于重新排列同源染色体之间的遗传信息很重要，并且对于它们正确的分离至关重要。COs沿染色体分布不均，控制CO定位的潜在机制还不清楚。我们先前显示，在没有AXR1的情况下，减数分裂的COs定位错误，而AXR1是拟南芥中参与neddylation / ruby​​lation蛋白修饰途径的一种酶。在这里，我们报告在axr1中^-/-，雄性肌细胞在染色体配对中显示出严重的缺陷，而端粒束的形成不受影响。与重组过程中耗尽的大中心区域相反，CO也会重新分配至端粒亚型染色体末端，在那里它们经常形成簇。CO抑制区域与axr1 ^{-/ -}减数分裂细胞CHH上下文中的转座因子（TEs）的DNA超甲基化相关。通过检查体细胞甲基化组，我们发现axr1 ^{-/ -}影响植物中的DNA甲基化，从而在TE的所有序列环境（CG，CHG和CHH）中引起超甲基化。DNA甲基化涉及的主要途径的损害是axr1上位的^{-/ -}用于体细胞DNA甲基化，但在减数分裂过程中不能恢复规则的染色体分离。总的来说，我们的发现表明，二联化途径不仅调节激素的感知和一氧化碳分布，而且还是直接或间接地在体细胞中TE DNA甲基化的主要限制途径。