Genetic diversity in offspring is induced by meiotic recombination, which is initiated between homologs at >200 sites originating from meiotic double-strand breaks (DSBs). Of this initial pool, only 1–2 DSBs per homolog pair will be designated to form meiotic crossovers (COs), where reciprocal genetic exchange occurs between parental chromosomes. Cyclin-dependent kinase 2 (CDK2) is known to localize to so-called “late recombination nodules” (LRNs) marking incipient CO sites. However, the role of CDK2 kinase activity in the process of CO formation remains uncertain. Here, we describe the phenotype of 2 Cdk2 point mutants with elevated or decreased activity, respectively. Elevated CDK2 activity was associated with increased numbers of LRN-associated proteins, including CDK2 itself and the MutL homolog 1 (MLH1) component of the MutLγ complex, but did not lead to increased numbers of COs. In contrast, reduced CDK2 activity leads to the complete absence of CO formation during meiotic prophase I. Our data suggest an important role for CDK2 in regulating MLH1 focus numbers and that the activity of this kinase is a key regulatory factor in the formation of meiotic COs.

后代的遗传多样性是由减数分裂重组诱导的，减数分裂重组起源于减数分裂双链断裂（DSB）的> 200个位点的同源物之间。在这个初始库中，每个同源对只有1-2个DSB被指定形成减数分裂交换（COs），亲代染色体之间发生相互的遗传交换。已知细胞周期蛋白依赖性激酶2（CDK2）定位于标记初始CO位点的所谓“晚期重组结节”（LRN）。然而，CDK2激酶活性在CO形成过程中的作用仍不确定。在这里，我们描述2 Cdk2的表型点突变体分别具有升高或降低的活性。CDK2活性升高与LRN相关蛋白的数量增加有关，包括CDK2本身和MutLγ复合体的MutL同源物1（MLH1）组分，但并未导致CO数量增加。相反，减少的CDK2活性导致在减数分裂前期I期间完全不形成CO。我们的数据表明CDK2在调节MLH1焦点数量中起重要作用，并且该激酶的活性是减数分裂COs形成的关键调控因子。