Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States of America.
Department of Biology, Wake Forest University, Winston-Salem, North Carolina, United States of America.
PLoS One. 2024 Mar 14;19(3):e0290672. doi: 10.1371/journal.pone.0290672. eCollection 2024.
Viral and cellular particles too large to freely diffuse have two different types of mobility in the eukaryotic cell cytoplasm: directed motion mediated by motor proteins moving along cytoskeletal elements with the particle as its load, and motion in random directions mediated by motor proteins interconnecting cytoskeletal elements. The latter motion is referred to as "active diffusion." Mechanisms of directed motion have been extensively studied compared to mechanisms of active diffusion, despite the observation that active diffusion is more common for many viral and cellular particles. Our previous research showed that active diffusion of vesicular stomatitis virus (VSV) ribonucleoproteins (RNPs) in the cytoplasm consists of hopping between traps and that actin filaments and myosin II motors are components of the hop-trap mechanism. This raises the question whether similar mechanisms mediate random motion of larger particles with different physical and biological properties. Live-cell fluorescence imaging and a variational Bayesian analysis used in pattern recognition and machine learning were used to determine the molecular mechanisms of random motion of VSV inclusion bodies and cellular early endosomes. VSV inclusion bodies are membraneless cellular compartments that are the major sites of viral RNA synthesis, and early endosomes are representative of cellular membrane-bound organelles. Like VSV RNPs, inclusion bodies and early endosomes moved from one trapped state to another, but the distance between states was inconsistent with hopping between traps, indicating that the apparent state-to-state movement is mediated by trap movement. Like VSV RNPs, treatment with the actin filament depolymerizing inhibitor latrunculin A increased VSV inclusion body mobility by increasing the size of the traps. In contrast neither treatment with latrunculin A nor depolymerization of microtubules by nocodazole treatment affected the size of traps that confine early endosome mobility, indicating that intermediate filaments are likely major trap components for these cellular organelles.
病毒和细胞颗粒太大,无法自由扩散,在真核细胞质中有两种不同类型的流动性:由沿着带有颗粒的细胞骨架元素移动的马达蛋白介导的定向运动,以及由连接细胞骨架元素的马达蛋白介导的随机方向运动。后者运动被称为“主动扩散”。与主动扩散相比,定向运动的机制已经得到了广泛的研究,尽管观察到主动扩散对于许多病毒和细胞颗粒更为常见。我们之前的研究表明,囊泡性口炎病毒 (VSV) 核糖核蛋白 (RNP) 在细胞质中的主动扩散由在陷阱之间跳跃组成,肌动蛋白丝和肌球蛋白 II 马达是跳跃-陷阱机制的组成部分。这就提出了一个问题,即是否有类似的机制介导具有不同物理和生物学特性的较大颗粒的随机运动。活细胞荧光成像和模式识别和机器学习中使用的变分贝叶斯分析用于确定 VSV 包涵体和细胞早期内体的随机运动的分子机制。VSV 包涵体是无膜的细胞区室,是病毒 RNA 合成的主要部位,早期内体是代表性的细胞膜结合细胞器。与 VSV RNPs 一样,包涵体和早期内体从一个被困状态移动到另一个状态,但状态之间的距离与跳跃到陷阱不相符,这表明明显的状态到状态的运动是由陷阱的运动介导的。与 VSV RNPs 一样,用肌动蛋白丝解聚抑制剂 latrunculin A 处理会通过增加陷阱的大小来增加 VSV 包涵体的流动性。相反,用 latrunculin A 处理或用 nocodazole 处理微管解聚都不会影响限制早期内体流动性的陷阱的大小,这表明中间丝可能是这些细胞细胞器的主要陷阱成分。