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Reconstitution reveals how myosin-VI self-organises to generate a dynamic mechanism of membrane sculpting

机译:重构揭示了肌球蛋白-VI如何自我组织以产生动态的膜雕刻机制

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摘要

One enigma in biology is the generation, sensing and maintenance of membrane curvature. Curvature-mediating proteins have been shown to induce specific membrane shapes by direct insertion and nanoscopic scaffolding, while the cytoskeletal motors exert forces indirectly through microtubule and actin networks. It remains unclear, whether the manifold direct motorprotein–lipid interactions themselves constitute another fundamental route to remodel the membrane shape. Here we show, combining super-resolution-fluorescence microscopy and membrane-reshaping nanoparticles, that curvature-dependent lipid interactions of myosin-VI on its own, remarkably remodel the membrane geometry into dynamic spatial patterns on the nano- to micrometer scale. We propose a quantitative theoretical model that explains this dynamic membrane sculpting mechanism. The emerging route of motorprotein–lipid interactions reshaping membrane morphology by a mechanism of feedback and instability opens up hitherto unexplored avenues of membrane remodelling and links cytoskeletal motors to early events in the sequence of membrane sculpting in eukaryotic cell biology.
机译:生物学中的一个谜是膜曲率的产生,感知和维持。已显示,通过直接插入和纳米支架,曲率介导的蛋白质可诱导特定的膜形状,而细胞骨架马达可通过微管和肌动蛋白网络间接施加作用力。尚不清楚歧管直接运动蛋白-脂质相互作用本身是否构成了重塑膜形状的另一基本途径。在这里,我们显示,结合超分辨率荧光显微镜和膜重塑纳米颗粒,肌球蛋白-VI自身依赖曲率的脂质相互作用,将膜几何学显着重塑为纳米级至微米级的动态空间模式。我们提出了一个定量的理论模型来解释这种动态的膜雕刻机制。运动蛋白-脂质相互作用通过反馈和不稳定性机制重塑膜形态的新兴途径打开了迄今为止尚未探索的膜重构途径,并将细胞骨架运动与真核细胞生物学中膜雕刻序列中的早期事件联系起来。

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