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通过 Arp2/3 复合物驱动的细胞质流在小鼠卵母细胞中动态维持不对称的减数分裂纺锤体位置。

Dynamic maintenance of asymmetric meiotic spindle position through Arp2/3-complex-driven cytoplasmic streaming in mouse oocytes.

机构信息

Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA.

出版信息

Nat Cell Biol. 2011 Aug 28;13(10):1252-8. doi: 10.1038/ncb2320.

DOI:10.1038/ncb2320
PMID:21874009
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3523671/
Abstract

Mature mammalian oocytes are poised for completing meiosis II (MII) on fertilization by positioning the spindle close to an actomyosin-rich cortical cap. Here, we show that the Arp2/3 complex localizes to the cortical cap in a Ran-GTPase-dependent manner and nucleates actin filaments in the cortical cap and a cytoplasmic actin network. Inhibition of Arp2/3 activity leads to rapid dissociation of the spindle from the cortex. Live-cell imaging and spatiotemporal image correlation spectroscopy analysis reveal that actin filaments flow continuously away from the Arp2/3-rich cortex, driving a cytoplasmic streaming expected to exert a net pushing force on the spindle towards the cortex. Arp2/3 inhibition not only diminishes this actin flow and cytoplasmic streaming but also enables a reverse streaming driven by myosin-II-based cortical contraction, moving the spindle away from the cortex. Thus, the asymmetric MII spindle position is dynamically maintained as a result of balanced forces governed by the Arp2/3 complex.

摘要

成熟的哺乳动物卵母细胞在受精时通过将纺锤体定位在富含肌动球蛋白的皮质帽附近,从而准备完成第二次减数分裂(MII)。在这里,我们表明 Arp2/3 复合物以依赖 Ran-GTPase 的方式定位于皮质帽,并在皮质帽和细胞质中的 actin 网络中引发 actin 丝的形成。Arp2/3 活性的抑制会导致纺锤体从皮质快速解离。活细胞成像和时空图像相关光谱分析揭示,actin 丝从富含 Arp2/3 的皮质连续流动,驱动细胞质流动,预计会对纺锤体向皮质施加净推力。Arp2/3 的抑制不仅会减少这种 actin 流动和细胞质流动,而且还会使基于肌球蛋白 II 的皮质收缩驱动反向流动,从而使纺锤体远离皮质。因此,不对称的 MII 纺锤体位置作为由 Arp2/3 复合物控制的平衡力的结果而被动态维持。

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