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在机械和化学刺激下细胞极性的逆转以及肌动蛋白-肌球蛋白细胞骨架的重组。

Reversal of cell polarity and actin-myosin cytoskeleton reorganization under mechanical and chemical stimulation.

作者信息

Dalous Jérémie, Burghardt Emmanuel, Müller-Taubenberger Annette, Bruckert Franz, Gerisch Günther, Bretschneider Till

机构信息

CEA-Grenoble, Département Réponse et Dynamique Cellulaires, Laboratoire de Biochimie et Biophysique des Systèmes Intégrés, Grenoble, France.

出版信息

Biophys J. 2008 Feb 1;94(3):1063-74. doi: 10.1529/biophysj.107.114702. Epub 2007 Sep 28.

Abstract

To study reorganization of the actin system in cells that invert their polarity, we stimulated Dictyostelium cells by mechanical forces from alternating directions. The cells oriented in a fluid flow by establishing a protruding front directed against the flow and a retracting tail. Labels for polymerized actin and filamentous myosin-II marked front and tail. At 2.1 Pa, actin first disassembled at the previous front before it began to polymerize at the newly induced front. In contrast, myosin-II slowly disappeared from the previous tail and continuously redistributed to the new tail. Front specification was myosin-II independent and accumulation of polymerized actin was even more focused in mutants lacking myosin-II heavy chains. We conclude that under mechanical stimulation, the inversion of cell polarity is initiated by a global internal signal that turns down actin polymerization in the entire cell. It is thought to be elicited at the most strongly stimulated site of the cell, the incipient front region, and to be counterbalanced by a slowly generated, short-range signal that locally activates actin polymerization at the front. Similar pattern of front and tail interconversion were observed in cells reorienting in strong gradients of the chemoattractant cyclic AMP.

摘要

为了研究极性反转细胞中肌动蛋白系统的重组,我们通过来自交替方向的机械力刺激盘基网柄菌细胞。细胞通过建立一个逆着流动方向突出的前端和一个回缩的后端来在流体流动中定向。聚合肌动蛋白和丝状肌球蛋白-II的标记物标记了前端和后端。在2.1帕斯卡时,肌动蛋白首先在前一个前端解聚,然后才开始在新诱导的前端聚合。相比之下,肌球蛋白-II从前一个后端缓慢消失,并持续重新分布到新的后端。前端的确定不依赖于肌球蛋白-II,并且在缺乏肌球蛋白-II重链的突变体中,聚合肌动蛋白的积累更加集中。我们得出结论,在机械刺激下,细胞极性的反转是由一个全局内部信号启动的,该信号降低了整个细胞中的肌动蛋白聚合。据认为,它在细胞受刺激最强的部位,即初始前端区域引发,并被一个缓慢产生的、短程信号抵消,该信号在前端局部激活肌动蛋白聚合。在趋化因子环磷酸腺苷的强梯度中重新定向的细胞中也观察到了类似的前端和后端相互转换模式。

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