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肌动球蛋白依赖性皮层动力学有助于果蝇胚胎早期的前期力平衡。

Actomyosin-dependent cortical dynamics contributes to the prophase force-balance in the early Drosophila embryo.

机构信息

Human Physiology Section, Department of Physiology, University of Pavia, Pavia, Italy.

出版信息

PLoS One. 2011 Mar 31;6(3):e18366. doi: 10.1371/journal.pone.0018366.

Abstract

BACKGROUND

The assembly of the Drosophila embryo mitotic spindle during prophase depends upon a balance of outward forces generated by cortical dynein and inward forces generated by kinesin-14 and nuclear elasticity. Myosin II is known to contribute to the dynamics of the cell cortex but how this influences the prophase force-balance is unclear.

PRINCIPAL FINDINGS

Here we investigated this question by injecting the myosin II inhibitor, Y27632, into early Drosophila embryos. We observed a significant increase in both the area of the dense cortical actin caps and in the spacing of the spindle poles. Tracking of microtubule plus ends marked by EB1-GFP and of actin at the cortex revealed that astral microtubules can interact with all regions of these expanded caps, presumably via their interaction with cortical dynein. In Scrambled mutants displaying abnormally small actin caps but normal prophase spindle length in late prophase, myosin II inhibition produced very short spindles.

CONCLUSIONS

These results suggest that two complementary outward forces are exerted on the prophase spindle by the overlying cortex. Specifically, dynein localized on the mechanically firm actin caps and the actomyosin-driven contraction of the deformable soft patches of the actin cortex, cooperate to pull astral microtubules outward. Thus, myosin II controls the size and dynamic properties of the actin-based cortex to influence the spacing of the poles of the underlying spindle during prophase.

摘要

背景

果蝇胚胎有丝分裂纺锤体在前期的组装取决于皮质动力蛋白产生的外向力和驱动蛋白-14 和核弹性产生的内向力之间的平衡。肌球蛋白 II 已知会影响细胞皮质的动力学,但它如何影响前期的力平衡尚不清楚。

主要发现

在这里,我们通过将肌球蛋白 II 抑制剂 Y27632 注入早期果蝇胚胎来研究这个问题。我们观察到致密皮质肌动蛋白帽的面积和纺锤体极的间距都显著增加。EB1-GFP 标记的微管末端和皮质处的肌动蛋白的追踪显示,星状微管可以与这些扩展帽的所有区域相互作用,可能是通过与皮质动力蛋白相互作用。在 Scrambled 突变体中,尽管致密的肌动蛋白帽异常小,但在后期前期纺锤体长度正常,肌球蛋白 II 抑制产生了非常短的纺锤体。

结论

这些结果表明,两个互补的外向力通过覆盖的皮质施加在前期纺锤体上。具体来说,定位于机械坚固的肌动蛋白帽上的动力蛋白和肌球蛋白驱动的肌动蛋白皮质的可变形软斑块的收缩,共同将星状微管向外拉动。因此,肌球蛋白 II 控制基于肌动蛋白的皮质的大小和动态特性,以影响前期基础纺锤体极的间距。

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