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分子到生物体的手性是由保守的肌球蛋白 1D 诱导的。

Molecular to organismal chirality is induced by the conserved myosin 1D.

机构信息

Université Côte D'Azur, CNRS, Inserm, Institut de Biologie Valrose, Nice, France.

Pennsylvania Muscle Institute and the Center for Engineering Mechanobiology, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, USA.

出版信息

Science. 2018 Nov 23;362(6417):949-952. doi: 10.1126/science.aat8642.

DOI:10.1126/science.aat8642
PMID:30467170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6698710/
Abstract

The emergence of asymmetry from an initially symmetrical state is a universal transition in nature. Living organisms show asymmetries at the molecular, cellular, tissular, and organismal level. However, whether and how multilevel asymmetries are related remains unclear. In this study, we show that myosin 1D (Myo1D) and myosin 1C (Myo1C) are sufficient to generate de novo directional twisting of cells, single organs, or the whole body in opposite directions. Directionality lies in the myosins' motor domain and is swappable between Myo1D and Myo1C. In addition, Myo1D drives gliding of actin filaments in circular, counterclockwise paths in vitro. Altogether, our results reveal the molecular motor Myo1D as a chiral determinant that is sufficient to break symmetry at all biological scales through chiral interaction with the actin cytoskeleton.

摘要

从最初对称的状态中出现的不对称是自然界中的一种普遍转变。生物体在分子、细胞、组织和机体水平上表现出不对称性。然而,多水平的不对称性是否以及如何相关尚不清楚。在这项研究中,我们表明肌球蛋白 1D(Myo1D)和肌球蛋白 1C(Myo1C)足以在相反方向上产生细胞、单个器官或整个身体的新的定向扭转。方向性在于肌球蛋白的运动域,并且可以在 Myo1D 和 Myo1C 之间交换。此外,Myo1D 在体外驱动肌动蛋白丝以圆形、逆时针路径滑行。总之,我们的结果揭示了分子马达 Myo1D 作为一个手性决定因素,通过与肌动蛋白细胞骨架的手性相互作用,足以在所有生物尺度上打破对称性。

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