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极光激酶 C 缺陷导致小鼠减数分裂 I 中的胞质分裂失败和大型多倍体卵母细胞的产生。

Aurora-C kinase deficiency causes cytokinesis failure in meiosis I and production of large polyploid oocytes in mice.

机构信息

Institute of Biomedical Sciences, Academia Sinica, Nankang, Taipei 115, Taiwan.

出版信息

Mol Biol Cell. 2010 Jul 15;21(14):2371-83. doi: 10.1091/mbc.e10-02-0170. Epub 2010 May 19.

DOI:10.1091/mbc.e10-02-0170
PMID:20484572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2903667/
Abstract

We previously isolated Aurora-C/Aie1 in a screen for kinases expressed in mouse sperm and eggs. Here, we show the localization of endogenous Aurora-C and examine its roles during female mouse meiosis. Aurora-C was detected at the centromeres and along the chromosome arms in prometaphase I-metaphase I and was concentrated at centromeres at metaphase II, in which Aurora-C also was phosphorylated at Thr171. During the anaphase I-telophase I transition, Aurora-C was dephosphorylated and relocalized to the midzone and midbody. Microinjection of the kinase-deficient Aurora-C (AurC-KD) mRNA into mouse oocytes significantly inhibited Aurora-C activity and caused multiple defects, including chromosome misalignment, abnormal kinetochore-microtubule attachment, premature chromosome segregation, and cytokinesis failure in meiosis I. Furthermore, AurC-KD reduced Aurora-C and histone H3 phosphorylation and inhibited kinetochore localization of Bub1 and BubR1. Similar effects also were observed in the oocytes injected with INCNEP-delIN mRNAs, in which the Aurora-C binding motif was removed. The most dramatic effect observed in AurC-KD-injected oocytes is cytokinesis failure in meiosis I, resulting in producing large polyploid oocytes, a pattern similar to Aurora-C deficiency human spermatozoa. Surprisingly, we detected no Aurora-B protein in mouse oocytes. We propose that Aurora-C, but not Aurora-B, plays essential roles in female mouse meiosis.

摘要

我们之前在一个筛选在小鼠精子和卵子中表达的激酶的实验中分离出 Aurora-C/Aie1。在这里，我们展示了内源性 Aurora-C 的定位，并研究了其在雌性小鼠减数分裂中的作用。在前期 I-中期 I 中，Aurora-C 定位于着丝粒和染色体臂上，在中期 II 中集中在着丝粒上，此时 Aurora-C 也在 Thr171 处被磷酸化。在后期 I-末期 I 过渡期间，Aurora-C 去磷酸化并重新定位到中体和中体。将激酶缺陷型 Aurora-C（AurC-KD）mRNA 微注射到小鼠卵母细胞中会显著抑制 Aurora-C 活性并导致多种缺陷，包括染色体错位、动粒-微管附着异常、染色体过早分离以及减数分裂 I 中的胞质分裂失败。此外，AurC-KD 减少了 Aurora-C 和组蛋白 H3 的磷酸化，并抑制了 Bub1 和 BubR1 在动粒上的定位。用去除了 Aurora-C 结合基序的 INCNEP-delIN mRNAs 注射的卵母细胞也观察到了类似的效果。在 AurC-KD 注射的卵母细胞中观察到的最显著的影响是减数分裂 I 中的胞质分裂失败，导致产生大的多倍体卵母细胞，这与 Aurora-C 缺乏的人类精子的模式相似。令人惊讶的是，我们在小鼠卵母细胞中未检测到 Aurora-B 蛋白。我们提出，Aurora-C 而不是 Aurora-B，在雌性小鼠减数分裂中发挥着重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cc5/2903667/f5e5b02d4e8d/zmk0141095090008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cc5/2903667/90b8c450283c/zmk0141095090002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cc5/2903667/f5e5b02d4e8d/zmk0141095090008.jpg

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