中期主轴稳定性和极向通量调节主轴长度的机制

IF 4.1 2区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES

iScience Pub Date : 2025-09-04 DOI:10.1016/j.isci.2025.113506

Yao Wang , Yu-Ru Liu , Peng-Ye Wang , Hui Li , Ping Xie

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引用次数: 0

摘要

在中期，纺锤体稳定染色体并保持其大小，尽管微管不断向两极流动。为了研究纺锤体稳定性的机制以及极性通量如何调节纺锤体的大小，我们建立了一个最小纺锤体模型，该模型包含着丝点、微管、纺锤极和微管滑动蛋白（如kinesin-5）、微管解聚蛋白（如kinesin-13）和微管交联蛋白（如NuMA）。我们发现，极性通量通过调节主轴长度和反平行微管重叠的长度来稳定主轴，从而实现微管滑动、正端聚合和负端解聚的相同速率。我们揭示了在小细胞中，极化通量如何与纺锤体长度和微管重叠长度成线性关系，以及微管成核如何影响大细胞中的纺锤体动力学的潜在机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Mechanism of spindle stability and poleward flux regulating spindle length during the metaphase

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Mechanism of spindle stability and poleward flux regulating spindle length during the metaphase

During metaphase, the spindle stabilizes chromosomes and maintains its size despite continuous microtubule poleward flux. To investigate the mechanism of the spindle stability and how the poleward flux regulates the spindle size, we establish a minimal spindle model that incorporates kinetochores, microtubules, spindle poles, and microtubule sliding proteins such as kinesin-5, microtubule depolymerizing proteins such as kinesin-13, and microtubule crosslinking proteins such as NuMA. We find that the poleward flux stabilizes the spindle by regulating the spindle length and the length of antiparallel microtubule overlaps to achieve equal rates of microtubule sliding, plus-end polymerization, and minus-end depolymerization. We reveal the underlying mechanism of how the poleward flux rate scales linearly with the spindle length and microtubule overlap length in small cells and how microtubule nucleation affects spindle dynamics in large cells.

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来源期刊

iScience Multidisciplinary-Multidisciplinary

CiteScore

7.20

自引率

1.70%

发文量

1972

审稿时长

6 weeks

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