Meiotic crossovers can be formed through the interfering pathway, in which one crossover prevents another from forming nearby, or by an independent non-interfering pathway. In Arabidopsis, local sequence polymorphism between homologs can stimulate interfering crossovers in a MSH2-dependent manner. To understand how MSH2 regulates crossovers formed by the two pathways, we combined Arabidopsis mutants that elevate non-interfering crossovers with msh2 mutants. We demonstrate that MSH2 blocks non-interfering crossovers at polymorphic loci, which is the opposite effect to interfering crossovers. We also observe MSH2-independent crossover inhibition at highly polymorphic sites. We measure recombination along the chromosome arms in lines differing in patterns of heterozygosity and observe a MSH2-dependent crossover increase at the boundaries between heterozygous and homozygous regions. Here, we show that MSH2 is a master regulator of meiotic DSB repair in Arabidopsis, with antagonistic effects on interfering and non-interfering crossovers, which shapes the crossover landscape in relation to interhomolog polymorphism.

减数分裂交叉可以通过干扰途径形成，其中一种交叉阻止附近形成另一种交叉，或者通过独立的非干扰途径形成。在拟南芥中，同源物之间的局部序列多态性可以以 MSH2 依赖性方式刺激干扰交叉。为了了解 MSH2 如何调节这两种途径形成的交叉，我们将提高非干扰交叉的拟南芥突变体与msh2突变体结合起来。我们证明 MSH2 会阻止多态性位点处的非干扰性交叉，这与干扰性交叉的效果相反。我们还在高度多态性位点观察到不依赖于 MSH2 的交叉抑制。我们测量了杂合性模式不同的染色体臂上的重组，并观察到杂合子和纯合子区域之间的边界处依赖于 MSH2 的交叉增加。在这里，我们证明 MSH2 是拟南芥减数分裂 DSB 修复的主要调节因子，对干扰和非干扰交叉具有拮抗作用，从而形成与同源间多态性相关的交叉景观。