Maternal RNA regulates Aurora C kinase during mouse oocyte maturation in a translation-independent fashion
Maternal RNA regulates Aurora C kinase during mouse oocyte maturation in a translation-independent fashion
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DOI：
10.1093/biolre/iox047
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发表时间：
2017-06-01
影响因子：
3.6
通讯作者：
Schindler, Karen
中科院分区：
文献类型：
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作者：
Balboula, Ahmed Z.;Blengini, Cecilia S.;Schindler, Karen
在卵母细胞减数分裂成熟过程中，极光激酶C（AURKC）需要完成许多关键功能，包括不稳定错误的着丝粒微管（K-MT）附件和调节双极纺锤体组装。然而，在哺乳动物卵母细胞中，AURKC的局部活性是如何调节的还不完全清楚。包括小鼠在内的许多物种的雌性配子含有下游发育事件所需的母体转录物。我们在这里表明，在小鼠卵母细胞中的母体RNA耗尽导致减数分裂进程受损，染色体错位和异常的纺锤体形成在中期I（Met I），和胞质分裂缺陷的发病率增加。重要的是，母体RNA的消耗扰乱了AURKC在染色体乘客复合体（CPC）内的定位和活性。这些扰动时，没有观察到翻译抑制放线菌酮（CHX）治疗。这些结果证明了母体RNA调节小鼠卵母细胞中AURKC-CPC功能的非依赖性功能。
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.Summary SentenceMaternal RNA contained in mouse oocytes regulates localized AURKC-CPC activity independent of its role in translation to support meiotic maturation.