Significance Successful chromosome segregation during meiosis relies on crossover recombination between homologous chromosomes. Meiotic recombination initiates with the formation of numerous DNA double-strand breaks, but only a few are ultimately selected to become crossovers. How this process is regulated to ensure that each homolog pair designates at least one crossover remains poorly understood. Here, we show that the Caenorhabditis elegans kinase CDK-2 partners with cyclin-like protein COSA-1 and promotes crossover designation through phosphorylation and activation of the MutSγ complex. Our data support a model in which scaffold-like properties of the MSH-5 C-terminal tail and its CDK-2–mediated phosphorylation combine to promote full recruitment and activity of crossover–promoting complexes, thereby generating positive feedback that contributes to the robustness of crossover designation.

Crossover formation is essential for proper segregation of homologous chromosomes during meiosis. Here we show that C. elegans Cyclin-dependent kinase 2 (CDK-2) forms a complex with cyclin-like protein COSA-1 and supports crossover formation by promoting conversion of meiotic double-strand breaks (DSBs) into crossover-specific recombination intermediates. Further, we identify MutSγ component MSH-5 as a CDK-2 phosphorylation target. MSH-5 has a disordered C-terminal tail that contains 13 potential CDK phosphosites and is required to concentrate crossover-promoting proteins at recombination sites. Phosphorylation of the MSH-5 tail appears dispensable in a wild-type background, but when MutSγ activity is partially compromised, crossover formation and retention of CDK-2/COSA-1 at recombination sites are exquisitely sensitive to phosphosite loss. Our data support a model in which robustness of crossover designation reflects a positive feedback mechanism involving CDK-2-mediated phosphorylation and scaffold-like properties of the MSH-5 C-terminal tail, features that combine to promote full recruitment and activity of crossover-promoting complexes.

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There is a strong relationship between accommodation ability and age. Accommodation ability decreases strongly from the 3rd to the 5th decade; after that the loss of accommodation ability is relatively lower. The increase in lens thickness during the life span can implicate a correlation between the change of anterior chamber depth in relation to the length of the eye and a decrease of accommodation ability. Our results confirm Duane's hypothesis of accommodation and age.