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本文引用的文献

1
Analysis of microtubule dynamic instability using a plus-end growth marker.使用微管正极生长标记物分析微管动态不稳定性。
Nat Methods. 2010 Sep;7(9):761-8. doi: 10.1038/nmeth.1493. Epub 2010 Aug 22.
2
Evidence for an upper limit to mitotic spindle length.有丝分裂纺锤体长度存在上限的证据。
Curr Biol. 2008 Aug 26;18(16):1256-61. doi: 10.1016/j.cub.2008.07.092.
3
Poleward transport of Eg5 by dynein-dynactin in Xenopus laevis egg extract spindles.在非洲爪蟾卵提取物纺锤体中,动力蛋白-动力蛋白激活蛋白介导Eg5向极运输。
J Cell Biol. 2008 Aug 25;182(4):715-26. doi: 10.1083/jcb.200801125. Epub 2008 Aug 18.
4
A novel small-molecule inhibitor reveals a possible role of kinesin-5 in anastral spindle-pole assembly.一种新型小分子抑制剂揭示了驱动蛋白-5在无星纺锤体极组装中的可能作用。
J Cell Sci. 2008 Jul 15;121(Pt 14):2293-300. doi: 10.1242/jcs.024018. Epub 2008 Jun 17.
5
Localized RanGTP accumulation promotes microtubule nucleation at kinetochores in somatic mammalian cells.局部RanGTP积累促进哺乳动物体细胞着丝粒处的微管成核。
Mol Biol Cell. 2008 May;19(5):1873-82. doi: 10.1091/mbc.e07-10-1050. Epub 2008 Feb 20.
6
Mechanisms of mitotic spindle assembly and function.有丝分裂纺锤体组装与功能的机制。
Int Rev Cytol. 2008;265:111-58. doi: 10.1016/S0074-7696(07)65003-7.
7
Architectural dynamics of the meiotic spindle revealed by single-fluorophore imaging.单荧光团成像揭示减数分裂纺锤体的结构动力学
Nat Cell Biol. 2007 Nov;9(11):1233-42. doi: 10.1038/ncb1643. Epub 2007 Oct 14.
8
Slide-and-cluster models for spindle assembly.纺锤体组装的滑动与聚类模型
Curr Biol. 2007 Aug 21;17(16):1373-83. doi: 10.1016/j.cub.2007.07.058.
9
Cooperative mechanisms of mitotic spindle formation.有丝分裂纺锤体形成的协同机制。
J Cell Sci. 2007 May 15;120(Pt 10):1717-22. doi: 10.1242/jcs.03442.
10
Xenopus tropicalis egg extracts provide insight into scaling of the mitotic spindle.热带爪蟾卵提取物为有丝分裂纺锤体的大小调控提供了见解。
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纺锤体融合需要动力蛋白介导的反向微管滑动。

Spindle fusion requires dynein-mediated sliding of oppositely oriented microtubules.

作者信息

Gatlin Jesse C, Matov Alexandre, Groen Aaron C, Needleman Daniel J, Maresca Thomas J, Danuser Gaudenz, Mitchison Timothy J, Salmon E D

机构信息

Marine Biological Laboratory, Woods Hole, MA 02543, USA.

出版信息

Curr Biol. 2009 Feb 24;19(4):287-96. doi: 10.1016/j.cub.2009.01.055.

DOI:10.1016/j.cub.2009.01.055
PMID:19230671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2709244/
Abstract

BACKGROUND

Bipolar spindle assembly is critical for achieving accurate segregation of chromosomes. In the absence of centrosomes, meiotic spindles achieve bipolarity by a combination of chromosome-initiated microtubule nucleation and stabilization and motor-driven organization of microtubules. Once assembled, the spindle structure is maintained on a relatively long time scale despite the high turnover of the microtubules that comprise it. To study the underlying mechanisms responsible for spindle assembly and steady-state maintenance, we used microneedle manipulation of preassembled spindles in Xenopus egg extracts.

RESULTS

When two meiotic spindles were brought close enough together, they interacted, creating an interconnected microtubule structure with supernumerary poles. Without exception, the perturbed system eventually re-established bipolarity, forming a single spindle of normal shape and size. Bipolar spindle fusion was blocked when cytoplasmic dynein function was perturbed, suggesting a critical role for the motor in this process. The fusion of Eg5-inhibited monopoles also required dynein function but only occurred if the initial interpolar separation was less than twice the microtubule radius of a typical monopole.

CONCLUSIONS

Our experiments uniquely illustrate the architectural plasticity of the spindle and reveal a robust ability of the system to attain a bipolar morphology. We hypothesize that a major mechanism driving spindle fusion is dynein-mediated sliding of oppositely oriented microtubules, a novel function for the motor, and posit that this same mechanism might also be involved in normal spindle assembly and homeostasis.

摘要

背景

双极纺锤体组装对于实现染色体的精确分离至关重要。在没有中心体的情况下,减数分裂纺锤体通过染色体引发的微管成核和稳定以及微管的马达驱动组织相结合来实现双极性。一旦组装完成,尽管构成纺锤体的微管周转速度很快,但纺锤体结构在相对较长的时间尺度上得以维持。为了研究纺锤体组装和稳态维持的潜在机制,我们在非洲爪蟾卵提取物中对预组装的纺锤体进行了微针操作。

结果

当两个减数分裂纺锤体靠得足够近时,它们会相互作用,形成一个具有多余极的相互连接的微管结构。无一例外,受干扰的系统最终会重新建立双极性,形成一个形状和大小正常的单个纺锤体。当细胞质动力蛋白功能受到干扰时,双极纺锤体融合被阻断,这表明该马达在这一过程中起关键作用。Eg5抑制的单极融合也需要动力蛋白功能,但只有当初始极间距离小于典型单极微管半径的两倍时才会发生。

结论

我们的实验独特地说明了纺锤体的结构可塑性,并揭示了该系统获得双极形态的强大能力。我们假设驱动纺锤体融合的一个主要机制是动力蛋白介导的相反方向微管的滑动,这是该马达的一种新功能,并推测这一相同机制可能也参与正常的纺锤体组装和稳态。