Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230026, China; College of Life Science and Technology, Southwest University of Science and Technology, Mianyang, Sichuan 621000, China.
Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230026, China.
Dev Biol. 2014 Aug 1;392(1):108-16. doi: 10.1016/j.ydbio.2014.04.018. Epub 2014 May 4.
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.
端粒簇集是真核生物中广泛存在的现象。然而，在哺乳动物减数分裂前期调节端粒簇集形成的分子机制在很大程度上仍然未知。在这里，我们表明 CDK2，特别是 p39(cdk2)，作为一种潜在的减数分裂特异性连接蛋白，与 SUN1 相互作用，介导了小鼠减数分裂中端粒簇集的形成。从 CDK2 到 p-CDK2 的转变也通过与 MLH1 相互作用调节了同源重组向解联的进展。此外，在 Sun1(-/-) 小鼠和粗线期阻滞杂种不育小鼠 (pwk×C57BL/6 F1) 中，分别观察到 CDK2 在端粒上的消失和 p-CDK2 在重组位点上的消失。这些结果表明，从 CDK2 到 p-CDK2 的转变对于调节减数分裂进程起着关键作用。
