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LIM Domains Target Actin Regulators Paxillin and Zyxin to Sites of Stress Fiber Strain

机译:LIM域将肌动蛋白调节剂Paxillin和Zyxin靶向应力纤维应变位点

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摘要

Contractile actomyosin stress fibers are critical for maintaining the force balance between the interior of the cell and its environment. Consequently, the actin cytoskeleton undergoes dynamic mechanical loading. This results in spontaneous, stochastic, highly localized strain events, characterized by thinning and elongation within a discrete region of stress fiber. Previous work showed the LIM-domain adaptor protein, zyxin, is essential for repair and stabilization of these sites. Using live imaging, we show paxillin, another LIM-domain adaptor protein, is also recruited to stress fiber strain sites. Paxillin recruitment to stress fiber strain sites precedes zyxin recruitment. Zyxin and paxillin are each recruited independently of the other. In cells lacking paxillin, actin recovery is abrogated, resulting in slowed actin recovery and increased incidence of catastrophic stress fiber breaks. For both paxillin and zyxin, the LIM domains are necessary and sufficient for recruitment. This work provides further evidence of the critical role of LIM-domain proteins in responding to mechanical stress in the actin cytoskeleton.
机译:收缩性肌动球蛋白应力纤维对于维持细胞内部与其环境之间的力量平衡至关重要。因此,肌动蛋白的细胞骨架受到动态的机械负荷。这导致了自发的,随机的,高度局部的应变事件,其特征是在应力纤维的离散区域内变薄和伸长。先前的工作表明,LIM结构域衔接子蛋白zyxin对于修复和稳定这些位点至关重要。使用实时成像,我们显示了另外一种LIM结构域衔接蛋白paxillin也被招募到应力纤维应变位点。将Paxillin募集到应力纤维应变位点之前先于zyxin募集。 Zyxin和paxillin各自独立招募。在缺乏paxillin的细胞中,肌动蛋白的恢复被取消,导致肌动蛋白的恢复减慢,灾难性应激纤维断裂的发生率增加。对于paxillin和zyxin,LIM域对于募集是必要和充分的。这项工作提供了进一步的证据,证明LIM结构域蛋白在响应肌动蛋白细胞骨架中的机械应激中的关键作用。

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