Physik Department E22, Technische Universität München, D-85748 Garching, Germany.
Arnold Sommerfeld Center for Theoretical Physics, Ludwig-Maximilians-Universität München, D-80333 München, Germany.
Proc Natl Acad Sci U S A. 2020 Feb 25;117(8):3944-3952. doi: 10.1073/pnas.1917964117. Epub 2020 Feb 10.
Cross-talk between the microtubule and actin networks has come under intense scrutiny following the realization that it is crucial for numerous essential processes, ranging from cytokinesis to cell migration. It is becoming increasingly clear that proteins long-considered highly specific for one or the other cytoskeletal system do, in fact, make use of both filament types. How this functional duality of "shared proteins" has evolved and how their coadaptation enables cross-talk at the molecular level remain largely unknown. We previously discovered that the mammalian adaptor protein melanophilin of the actin-associated myosin motor is one such "shared protein," which also interacts with microtubules in vitro. In a hypothesis-driven in vitro and in silico approach, we turn to early and lower vertebrates and ask two fundamental questions. First, is the capability of interacting with microtubules and actin filaments unique to mammalian melanophilin or did it evolve over time? Second, what is the functional consequence of being able to interact with both filament types at the cellular level? We describe the emergence of a protein domain that confers the capability of interacting with both filament types onto melanophilin. Strikingly, our computational modeling demonstrates that the regulatory power of this domain on the microscopic scale alone is sufficient to recapitulate previously observed behavior of pigment organelles in amphibian melanophores. Collectively, our dissection provides a molecular framework for explaining the underpinnings of functional cross-talk and its potential to orchestrate the cell-wide redistribution of organelles on the cytoskeleton.
在认识到细胞分裂到细胞迁移等众多基本过程都依赖于微管和肌动蛋白网络之间的串扰之后,人们对其进行了深入研究。越来越明显的是,长期以来被认为高度特异性地存在于一种细胞骨架系统中的蛋白质实际上确实利用了这两种纤维类型。这种“共享蛋白”的功能双重性是如何进化的,以及它们的共同适应如何在分子水平上实现串扰,在很大程度上仍然未知。我们之前发现,肌球蛋白马达相关的肌动蛋白结合蛋白黑素磷蛋白是这样的“共享蛋白”之一,它在体外也与微管相互作用。在一个基于假设的体外和计算机模拟方法中,我们转向早期和低等脊椎动物,并提出两个基本问题。首先,与微管和肌动蛋白丝相互作用的能力是哺乳动物黑素磷蛋白所特有的,还是随着时间的推移而进化的?其次,在细胞水平上能够与两种纤维类型相互作用的功能后果是什么?我们描述了一个蛋白质结构域的出现,该结构域赋予了黑素磷蛋白与两种纤维类型相互作用的能力。引人注目的是,我们的计算模型表明,仅在微观尺度上,该结构域的调节能力就足以再现先前在两栖动物黑素细胞中观察到的色素细胞器的行为。总的来说,我们的剖析为解释功能串扰的基础及其在细胞骨架上协调细胞器的全细胞重新分布的潜力提供了一个分子框架。