Yang Kuo-Tai, Tang Chieh-Ju C, Tang Tang K
Department of Animal Science and Technology, National Taiwan University , Taipei , Taiwan.
Institute of Biomedical Sciences, Academia Sinica , Taipei , Taiwan.
Front Oncol. 2015 Aug 13;5:178. doi: 10.3389/fonc.2015.00178. eCollection 2015.
The meiotic generation of haploid gametes with equal contents of genetic material is important for sexual reproduction in mammals. Errors in the transmission of chromosomes during meiosis may lead to aneuploidy, which is the leading cause of miscarriage and congenital birth defects in humans. The Aurora kinases, which include Aurora-A, Aurora-B, and Aurora-C, are highly conserved serine-threonine kinases that play essential roles in centrosome function, chromosome segregation, and cytokinesis during mitosis and meiosis. While Aurora-A and Aurora-B have been extensively studied in mitosis, the role of Aurora-C in meiosis is only now starting to be revealed. For example, the perturbation of Aurora-C kinase activity by microinjection of Aurora-C-kinase-dead mutant mRNAs into mouse oocytes induced multiple defects, including chromosome misalignment, abnormal kinetochore-microtubule attachment, premature chromosome segregation, and failure of cytokinesis during meiotic division. However, the analysis of such defects is complicated by the possibility that Aurora-B may be present in mammalian germ cells. Interestingly, a homozygous mutation of Aurora-C in humans leads to the production of large-headed polyploid spermatozoa and causes male infertility, but homozygous females are fertile. Mouse studies regarding the roles of Aurora-B and Aurora-C in female meiotic divisions have yielded inconsistent results, and it has proven difficult to explain why homozygous human females have no significant clinical phenotype. In this review, we will discuss the controversial status of Aurora-B in oocytes and the possible role of Aurora-C during meiotic division.
减数分裂产生具有等量遗传物质的单倍体配子对于哺乳动物的有性生殖至关重要。减数分裂过程中染色体传递错误可能导致非整倍体，这是人类流产和先天性出生缺陷的主要原因。极光激酶包括极光-A、极光-B和极光-C，是高度保守的丝氨酸-苏氨酸激酶，在有丝分裂和减数分裂过程中的中心体功能、染色体分离和胞质分裂中起重要作用。虽然极光-A和极光-B在有丝分裂中已被广泛研究，但极光-C在减数分裂中的作用才刚刚开始被揭示。例如，通过向小鼠卵母细胞显微注射极光-C激酶失活突变体mRNA来干扰极光-C激酶活性会导致多种缺陷，包括染色体排列错误、动粒-微管附着异常、染色体过早分离以及减数分裂期间胞质分裂失败。然而，由于极光-B可能存在于哺乳动物生殖细胞中，对这些缺陷的分析变得复杂。有趣的是，人类中极光-C的纯合突变会导致大头多倍体精子的产生并导致男性不育，但纯合女性是可育的。关于极光-B和极光-C在雌性减数分裂中的作用的小鼠研究结果并不一致，并且很难解释为什么纯合人类女性没有明显的临床表型。在这篇综述中，我们将讨论极光-B在卵母细胞中的争议地位以及极光-C在减数分裂期间可能的作用。
