DNA运输由主动微管动力学进行拓扑塑造
DNA transport is topologically sculpted by active microtubule dynamics
AI总结：
本文利用单分子追踪研究线性与环状DNA在主动微管网络中的运输，发现DNA拓扑结构显著影响非高斯多模态运输行为，环状DNA因微管穿环而表现出增强亚扩散或超扩散，为编程分子运输和设计仿生材料提供新机制。
摘要：
大分子（如DNA）通过细胞骨架的运输对从细胞质环流到转录等广泛的细胞过程至关重要。由构成细胞骨架的细丝网络所赋予的刚性和空间位阻通常导致反常亚扩散，而主动过程（如马达驱动的重构）可诱导非热超扩散。理解这些看似对立的贡献在细胞内动力学中的相互作用仍然是一项重大挑战。在此，我们使用单分子追踪表明，大型线性和环状DNA通过马达驱动的微管网络的运输可以是非高斯和多模态的，这些特征表现的程度和时空尺度非平凡地取决于活性状态和DNA拓扑结构。例如，主动网络重构增加了线性DNA的笼闭和非高斯运输模式，同时抑制了环状DNA的这些机制。我们进一步发现，与线性对应物相比，环状DNA分子在不存在或存在驱动蛋白活性的情况下分别表现出显著增强的亚扩散或超扩散，表明微管穿过了环状DNA。这种强耦合导致停滞和定向运输，为解析运输的不同贡献并确定耦合对运输特征的影响提供了一条直接途径。更广泛地说，利用大分子拓扑结构作为编程分子相互作用和运输动力学的途径，是一种优雅但在很大程度上被忽视的机制，细胞可能利用该机制进行细胞内运输、环流和区室化。这种机制可用于设计自调节、传感和可重构的仿生物质。
英文摘要：
The transport of macromolecules, such as DNA, through the cytoskeleton is critical to wide-ranging cellular processes from cytoplasmic streaming to transcription. The rigidity and steric hindrances imparted by the network of filaments comprising the cytoskeleton often leads to anomalous subdiffusion, while active processes such as motor-driven restructuring can induce athermal superdiffusion. Understanding the interplay between these seemingly antagonistic contributions to intracellular dynamics remains a grand challenge. Here, we use single-molecule tracking to show that the transport of large linear and circular DNA through motor-driven microtubule networks can be non-gaussian and multi-modal, with the degree and spatiotemporal scales over which these features manifest depending non-trivially on the state of activity and DNA topology. For example, active network restructuring increases caging and non-Gaussian transport modes of linear DNA, while dampening these mechanisms for rings. We further discover that circular DNA molecules exhibit either markedly enhanced subdiffusion or superdiffusion compared to their linear counterparts, in the absence or presence of kinesin activity, indicative of microtubules threading circular DNA. This strong coupling leads to both stalling and directed transport, providing a direct route towards parsing distinct contributions to transport and determining the impact of coupling on the transport signatures. More generally, leveraging macromolecular topology as a route to programming molecular interactions and transport dynamics is an elegant yet largely overlooked mechanism that cells may exploit for intracellular trafficking, streaming, and compartmentalization. This mechanism could be harnessed for the design of self-regulating, sensing, and reconfigurable biomimetic matter.
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