A feature of metazoan reproduction is the elimination of maternal centrosomes from the oocyte. In animals that form syncytial cysts during oogenesis, including Drosophila and human, all centrosomes within the cyst migrate to the oocyte where they are subsequently degenerated. The importance and the underlying mechanism of this event remain unclear. Here, we show that, during early Drosophila oogenesis, control of the Anaphase Promoting Complex/Cyclosome (APC/C), the ubiquitin ligase complex essential for cell cycle control, ensures proper transport of centrosomes into the oocyte through the regulation of Polo/Plk1 kinase, a critical regulator of the integrity and activity of the centrosome. We show that novel mutations in the APC/C-specific E2, Vihar/Ube2c, that affect its inhibitory regulation on APC/C cause precocious Polo degradation and impedes centrosome transport, through destabilization of centrosomes. The failure of centrosome migration correlates with weakened microtubule polarization in the cyst and allows ectopic microtubule nucleation in nurse cells, leading to the loss of oocyte identity. These results suggest a role for centrosome migration in oocyte fate maintenance through the concentration and confinement of microtubule nucleation activity into the oocyte. Considering the conserved roles of APC/C and Polo throughout the animal kingdom, our findings may be translated into other animals.

后生动物繁殖的一个特征是从卵母细胞中消除母体中心体。在卵子发生过程中形成合胞体囊肿的动物中，包括果蝇和人类，囊肿内的所有中心体都迁移到卵母细胞，随后在那里发生退化。该事件的重要性和潜在机制仍不清楚。在这里，我们表明，在果蝇早期卵子发生，控制后期促进复合物/细胞周期小体 (APC/C)，泛素连接酶复合物对细胞周期控制至关重要，通过调节 Polo/Plk1 激酶确保中心体正确转运到卵母细胞中，Polo/Plk1 激酶是完整性的关键调节剂中心体的活性。我们表明，APC/C 特异性 E2、Vihar/Ube2c 中的新突变会影响其对 APC/C 的抑制调节，从而导致早熟的 Polo 降解并通过中心体的不稳定来阻碍中心体运输。中心体迁移的失败与包囊中微管极化减弱相关，并允许滋养细胞中的异位微管成核，从而导致卵母细胞特性的丧失。这些结果表明，通过将微管成核活动集中和限制到卵母细胞中，中心体迁移在卵母细胞命运维持中发挥作用。考虑到 APC/C 和 Polo 在整个动物界的保守作用，我们的发现可能会转化为其他动物。