Phosphorylation of CDK2 at threonine 160 regulates meiotic pachytene and diplotene progression in mice

• DOI: 10.1016/j.ydbio.2014.04.018
• Publication Date: 2014-05-04T18:47:33Z
• Authors: Wenjing Liu; Lu Wang; Weidong Zhao; Gendi Song; Rener Xu; Guishuan Wang; Fei Wang; Wenqing Li; Jie Lian; Hui Tian; Xiaorong Wang; Fei Sun
• Keywords: Male; Mouse; p39cdk2/p-CDK2; Mice; 03 medical and health sciences; Animals; Meiotic Prophase I; Phosphorylation; Molecular Biology; Infertility, Male; Adaptor Proteins, Signal Transducing; Mice, Knockout; 0303 health sciences; Telomere clustering; Cyclin-Dependent Kinase 2; MLH1; Nuclear Proteins; Synapsis; Cell Biology; Telomere; Recombination; Mice, Inbred C57BL; Meiosis; SUN1; Pachytene Stage; MutL Protein Homolog 1; Microtubule-Associated Proteins; Developmental Biology

Telomere clustering is a widespread phenomenon among eukaryotes. However, the molecular mechanisms that regulate formation of telomere clustering in mammalian meiotic prophase I, are still largely unknown. Here, we show that CDK2, especially p39(cdk2), as a potential meiosis-specific connector interaction with SUN1 mediates formation of telomere clustering during mouse meiosis. The transition from CDK2 to p-CDK2 also regulates the progression from homologous recombination to desynapsis by interacting with MLH1. In addition, disappearance of CDK2 on the telomeres and of p-CDK2 on recombination sites, were observed in Sun1(-/-) mice and in pachytene-arrested hybrid sterile mice (pwk×C57BL/6 F1), respectively. These results suggest that transition from CDK2 to p-CDK2 plays a critical role for regulating meiosis progression.