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首页> 外文期刊>Cell cycle >Emi1 class of proteins regulate entry into meiosis and the meiosis I to meiosis II transition in Xenopus oocytes.
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Emi1 class of proteins regulate entry into meiosis and the meiosis I to meiosis II transition in Xenopus oocytes.

机译：Emi1类蛋白质可调节非洲爪蟾卵母细胞进入减数分裂的过程以及减数分裂I向减数分裂II的转变。

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摘要

Xenopus oocytes are arrested at the G2/prophase boundary of meiosis I and enter meiosis in response to progesterone. A hallmark of meiosis is the absence of DNA replication between the successive cell division phases meiosis I (MI) and meiosis II (MII). After the MI-MII transition, Xenopus eggs are locked in metaphase II by the cytostatic factor (CSF) arrest to prevent parthenogenesis. Early Mitotic Inhibitor 1 (Emi1) maintains CSF arrest by inhibiting the ability of the Anaphase Promoting Complex (APC) to direct the destruction of cyclin B. To investigate whether Emi1 has an earlier role in meiosis, we injected Xenopus oocytes with neutralizing antibodies against Emi1 at G2/prophase and during the MI-MII transition. Progesterone-treated G2/prophase oocytes injected with anti-Emi1 antibody fail to activate Maturation Promoting Factor (MPF), a complex of cdc2/cyclin B, and the MAPK pathway, and do not undergo germinal vesicle breakdown (GVBD). Injection of purified Delta90 cyclin B protein or blocking anti-Emi1 antibody with purified Emi1 protein rescues these meiotic processes in Emi1-neutralized oocytes. Acute inhibition of Emi1 in progesterone treated oocytes immediately after GVBD causes rapid loss of cdc2 activity with simultaneous loss of cyclin B levels and inactivation of the MAPK pathway. These oocytes decondense their chromosomes and enter a DNA replication phase instead of progressing to MII. Prior ablation of Cdc20, addition of methyl-ubiquitin, or addition of nondestructible Delta90 cyclin B rescues the MI-MII transition in Emi1-inhibited oocytes.
机译：爪蟾卵母细胞停在减数分裂I的G2 /前期边界，并响应孕酮进入减数分裂。减数分裂的标志是在连续的细胞分裂期减数分裂I（MI）和减数分裂II（MII）之间不存在DNA复制。 MI-MII过渡后，爪蟾卵被抑制细胞生长因子（CSF）锁定在中期II，以防止孤雌生殖。早期有丝分裂抑制剂1（Emi1）通过抑制后期促进复合物（APC）指导细胞周期蛋白B破坏的能力来维持CSF阻滞。为了研究Emi1在减数分裂中是否具有更早的作用，我们向非洲爪蟾卵母细胞注射了抗Emi1的中和抗体在G2 /前期和MI-MII过渡期间。注射抗Emi1抗体的孕酮处理过的G2 /前卵母细胞无法激活成熟促进因子（MPF），cdc2 / cyclin B的复合物和MAPK途径，并且不会经历生小泡破坏（GVBD）。注射纯化的Delta90细胞周期蛋白B蛋白或用纯化的Emi1蛋白阻断抗Emi1抗体可挽救Emi1中和的卵母细胞的这些减数分裂过程。 GVBD后立即对经孕激素处理的卵母细胞中的Emi1进行急性抑制会导致cdc2活性快速丧失，同时细胞周期蛋白B水平降低和MAPK途径失活。这些卵母细胞使它们的染色体缩聚并进入DNA复制阶段，而不是发展为MII。预先消融Cdc20，添加甲基遍在蛋白或添加不可破坏的Delta90细胞周期蛋白B可以挽救Emi1抑制的卵母细胞中MI-MII的转变。

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