In mammals, oocytes are arrested in prophase of meiosis I for long periods of time. Prophase arrest is critical for reproduction because it allows oocytes to grow to their full size to support meiotic maturation and embryonic development. Prophase arrest requires the inhibitory phosphorylation of the mitotic kinase CDK1. Whether prophase arrest is also regulated at the translational level is unknown. Here, we show that prophase arrest is regulated by translational control of dormant cyclin B1 mRNAs. Using Trim-Away, we identify two mechanisms that maintain cyclin B1 dormancy and thus prophase arrest. First, a complex of the RNA-binding proteins DDX6, LSM14B and CPEB1 directly represses cyclin B1 translation through interacting with its 3’UTR. Second, cytoplasmic poly(A)-binding proteins (PABPCs) indirectly repress the translation of cyclin B1 and other poly(A)-tail-less or short-tailed mRNAs by sequestering the translation machinery on long-tailed mRNAs. Together, we demonstrate how RNA-binding proteins coordinately regulate prophase arrest, and reveal an unexpected role for PABPCs in controlling mRNA dormancy.

在哺乳动物中，卵母细胞长时间停滞在减数分裂 I 的前期。前期停滞对生殖至关重要，因为它允许卵母细胞生长到其完整大小以支持减数分裂成熟和胚胎发育。前期停滞需要有丝分裂激酶 CDK1 的抑制性磷酸化。前期停滞是否也在翻译水平上受到调节尚不清楚。在这里，我们表明前期停滞受休眠细胞周期蛋白 B1 mRNA 的翻译控制调节。使用 Trim-Away，我们确定了维持细胞周期蛋白 B1 休眠并因此停滞前期的两种机制。首先，RNA 结合蛋白 DDX6、LSM14B 和 CPEB1 的复合物通过与细胞周期蛋白 B1 的 3'UTR 相互作用直接抑制细胞周期蛋白 B1 翻译。其次，细胞质 poly （A） 结合蛋白 （PABPC） 通过隔离长尾 mRNA 上的翻译机制，间接抑制细胞周期蛋白 B1 和其他 poly（A） 无尾或短尾 mRNA 的翻译。我们一起展示了 RNA 结合蛋白如何协调调节前期停滞，并揭示了 PABPCs 在控制 mRNA 休眠中的意想不到的作用。