Laboratory of Chromosome Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.
Laboratory of Chromosome Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.
Dev Cell. 2017 Jan 9;40(1):37-52. doi: 10.1016/j.devcel.2016.11.021. Epub 2016 Dec 22.
Meiosis consists of DNA replication followed by two consecutive nuclear divisions and gametogenesis or spore formation. While meiosis I has been studied extensively, less is known about the regulation of meiosis II. Here we show that Hrr25, the conserved casein kinase 1δ of budding yeast, links three mutually independent key processes of meiosis II. First, Hrr25 induces nuclear division by priming centromeric cohesin for cleavage by separase. Hrr25 simultaneously phosphorylates Rec8, the cleavable subunit of cohesin, and removes from centromeres the cohesin protector composed of shugoshin and the phosphatase PP2A. Second, Hrr25 initiates the sporulation program by inducing the synthesis of membranes that engulf the emerging nuclei at anaphase II. Third, Hrr25 mediates exit from meiosis II by activating pathways that trigger the destruction of M-phase-promoting kinases. Thus, Hrr25 synchronizes formation of the single-copy genome with gamete differentiation and termination of meiosis.
减数分裂包括 DNA 复制，随后是两次连续的核分裂和配子发生或孢子形成。虽然减数分裂 I 已经被广泛研究，但减数分裂 II 的调控机制知之甚少。在这里，我们表明，芽殖酵母中保守的酪蛋白激酶 1δ（Casein kinase 1δ）Hrr25 连接了减数分裂 II 的三个相互独立的关键过程。首先，Hrr25 通过促使着丝粒黏合蛋白被分离酶切割来诱导核分裂。Hrr25 同时磷酸化 Rec8，即黏合蛋白的可切割亚基，并将由 Shugoshin 和磷酸酶 PP2A 组成的黏合蛋白保护因子从着丝粒上移除。其次，Hrr25 通过诱导吞噬即将形成的核的膜的合成，启动孢子形成程序。第三，Hrr25 通过激活触发 M 期促进激酶破坏的途径，介导减数分裂 II 的退出。因此，Hrr25 使单拷贝基因组的形成与配子分化和减数分裂的终止同步。
