Extent of myosin penetration within the actin cortex regulates cell surface mechanics.
Extent of myosin penetration within the actin cortex regulates cell surface mechanics.
复制标题
肌球蛋白在肌动蛋白皮质内的渗透程度调节细胞表面力学。
DOI：
10.1038/s41467-021-26611-2
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发表时间：
2021-11-11
影响因子：
16.6
通讯作者：
Paluch EK
中科院分区：
文献类型：
--
作者：
Truong Quang BA;Peters R;Cassani DAD;Chugh P;Clark AG;Agnew M;Charras G;Paluch EK
在动物细胞中，形状主要是由肌动球蛋白皮质决定的，肌动球蛋白皮质是质膜下面的薄细胞骨架网络。肌球蛋白马达在皮质中产生张力，张力梯度导致细胞变形。因此，许多细胞形态发生研究集中在控制肌球蛋白活性和向皮质募集的机制上。在这里，我们证明了使用超分辨率显微镜，肌球蛋白并不总是与肌动蛋白在皮层重叠，但仍然限制对细胞质中的低皮质张力。我们建议，这种限制性的渗透结果从空间位阻，肌球蛋白微丝是相当大的比皮层肌动蛋白meshsize。我们确定肌球蛋白的活性和肌动蛋白网络结构的肌球蛋白渗透到皮层的关键调节，并表明，增加肌球蛋白渗透增加皮质张力。我们的研究表明，在皮层的肌球蛋白和肌动蛋白的空间协调调节细胞表面力学，并揭示了一个重要的机制，肌球蛋白的大小控制其行动，通过限制微丝渗透到皮层肌动蛋白网络。更一般地说，我们的研究结果表明，蛋白质的大小可以调节致密的细胞骨架结构的功能。细胞变形主要是由膜下肌动蛋白皮质中的肌球蛋白马达产生的收缩力驱动的。在这里，我们表明，这些力量不仅是由皮质肌球蛋白水平控制，而是由肌球蛋白的空间排列，特别是它们与皮质肌动蛋白重叠的程度。
In animal cells, shape is mostly determined by the actomyosin cortex, a thin cytoskeletal network underlying the plasma membrane. Myosin motors generate tension in the cortex, and tension gradients result in cellular deformations. As such, many cell morphogenesis studies have focused on the mechanisms controlling myosin activity and recruitment to the cortex. Here, we demonstrate using super-resolution microscopy that myosin does not always overlap with actin at the cortex, but remains restricted towards the cytoplasm in cells with low cortex tension. We propose that this restricted penetration results from steric hindrance, as myosin minifilaments are considerably larger than the cortical actin meshsize. We identify myosin activity and actin network architecture as key regulators of myosin penetration into the cortex, and show that increasing myosin penetration increases cortical tension. Our study reveals that the spatial coordination of myosin and actin at the cortex regulates cell surface mechanics, and unveils an important mechanism whereby myosin size controls its action by limiting minifilament penetration into the cortical actin network. More generally, our findings suggest that protein size could regulate function in dense cytoskeletal structures. Cellular deformations are largely driven by contractile forces generated by myosin motors in the submembraneous actin cortex. Here we show that these forces are controlled not simply by cortical myosin levels, but rather by myosins spatial arrangement, specifically the extent of their overlap with cortical actin.
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影响因子：
3.3
作者：
Henson JH;Ditzler CE;Germain A;Irwin PM;Vogt ET;Yang S;Wu X;Shuster CB
通讯作者：
Shuster CB
影响因子：
4
作者：
Chugh P;Paluch EK
通讯作者：
Paluch EK
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通讯作者：
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作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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