The septin cytoskeleton facilitates membrane retraction during motility and blebbing.

The septin cytoskeleton facilitates membrane retraction during motility and blebbing.
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SEPTIN细胞骨架有助于在运动和爆炸期间膜回缩。

DOI:
10.1083/jcb.201105127
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发表时间:
2012-01-09
期刊:
The Journal of cell biology
影响因子:
--
通讯作者:
Krummel MF
Krummel MF
中科院分区:
其他
文献类型:
--
作者:
Gilden JK;Peck S;Chen YC;Krummel MF

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隔蛋白聚集在皮质上,通过收缩异常突出的膜并在变形虫运动过程中促进皮质收缩,恢复正常的细胞形状。越来越多的证据支持细胞膜上的隔膜细胞骨架在包括运动、树突棘或纤毛的形成和吞噬等生理过程中起着关键作用。我们试图确定间隔蛋白如何调节质膜,重点是这种细胞骨架元件在有效的阿米巴运动中的作用。令人惊讶的是,Septins扮演的是反应性而不是主动性的角色,在对不断增加的静水压力和随后的调节量减少的反应中证明了这一点。在这些环境中,快速的皮质收缩需要间隔蛋白,而SEPT6-GFP在整体皮质收缩期间,特别是在肌动蛋白细丝耗尽期间,被招募到细丝和圆形斑块中。在用动力蛋白抑制剂阻断膜运输而引发的过度起泡过程中,也明显地发现了Septins的招募,这进一步证明在动态形状变化期间,Septins被招募以促进膜的回缩。这种在不稳定的皮质上聚集和收缩异常突出的膜的功能解释了在缺乏Septin的T细胞中观察到的过多的起泡和突出。
Septins assemble on the cortex and restore normal cell shape by retracting aberrantly protruding membranes and promoting cortical contraction during amoeboid motility. Increasing evidence supports a critical role for the septin cytoskeleton at the plasma membrane during physiological processes including motility, formation of dendritic spines or cilia, and phagocytosis. We sought to determine how septins regulate the plasma membrane, focusing on this cytoskeletal element’s role during effective amoeboid motility. Surprisingly, septins play a reactive rather than proactive role, as demonstrated during the response to increasing hydrostatic pressure and subsequent regulatory volume decrease. In these settings, septins were required for rapid cortical contraction, and SEPT6-GFP was recruited into filaments and circular patches during global cortical contraction and also specifically during actin filament depletion. Recruitment of septins was also evident during excessive blebbing initiated by blocking membrane trafficking with a dynamin inhibitor, providing further evidence that septins are recruited to facilitate retraction of membranes during dynamic shape change. This function of septins in assembling on an unstable cortex and retracting aberrantly protruding membranes explains the excessive blebbing and protrusion observed in septin-deficient T cells.
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