Balboula Ahmed Z, Blengini Cecilia S, Gentilello Amanda S, Takahashi Masashi, Schindler Karen
Department of Genetics, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA.
Department of Animal Science, Graduate school of Agriculture, Hokkaido University, Sapporo, Hokkaido, Japan.
Biol Reprod. 2017 Jun 1;96(6):1197-1209. doi: 10.1093/biolre/iox047.
During oocyte meiotic maturation, Aurora kinase C (AURKC) is required to accomplish many critical functions including destabilizing erroneous kinetochore-microtubule (K-MT)attachments and regulating bipolar spindle assembly. How localized activity of AURKC is regulated in mammalian oocytes, however, is not fully understood. Female gametes from many species, including mouse, contain stores of maternal transcripts that are required for downstream developmental events. We show here that depletion of maternal RNA in mouse oocytes resulted in impaired meiotic progression, increased incidence of chromosome misalignment and abnormal spindle formation at metaphase I (Met I), and cytokinesis defects. Importantly, depletion of maternal RNA perturbed the localization and activity of AURKC within the chromosomal passenger complex (CPC). These perturbations were not observed when translation was inhibited by cycloheximide (CHX) treatment. These results demonstrate a translation-independent function of maternal RNA to regulate AURKC-CPC function in mouse oocytes.
在卵母细胞减数分裂成熟过程中，极光激酶C（AURKC）对于完成许多关键功能是必需的，包括破坏错误的动粒-微管（K-MT）附着以及调节双极纺锤体组装。然而，AURKC的局部活性在哺乳动物卵母细胞中是如何被调节的，目前尚未完全清楚。包括小鼠在内的许多物种的雌配子都含有母体转录本库，这些转录本对于下游发育事件是必需的。我们在此表明，小鼠卵母细胞中母体RNA的缺失导致减数分裂进程受损、染色体排列错误的发生率增加以及中期I（Met I）时纺锤体形成异常，还有胞质分裂缺陷。重要的是，母体RNA的缺失扰乱了AURKC在染色体乘客复合体（CPC）中的定位和活性。当用环己酰亚胺（CHX）处理抑制翻译时，未观察到这些扰动。这些结果证明了母体RNA在调节小鼠卵母细胞中AURKC-CPC功能方面具有不依赖翻译的功能。
