Laboratoire de Physiologie Cellulaire et Végétale, Institut de Recherches en Technologies et Sciences pour le Vivant, UMR CNRS, CEA, INRA, Université Joseph Fourier, 38054 Grenoble, France.
Mol Biol Cell. 2013 Jun;24(12):1964-73. doi: 10.1091/mbc.E13-03-0141. Epub 2013 Apr 24.
Microtubules (MTs) are dynamic cytoskeletal elements involved in numerous cellular processes. Although they are highly rigid polymers with a persistence length of 1-8 mm, they may exhibit a curved shape at a scale of few micrometers within cells, depending on their biological functions. However, how MT flexural rigidity in cells is regulated remains poorly understood. Here we ask whether MT-associated proteins (MAPs) could locally control the mechanical properties of MTs. We show that two major cross-linkers of the conserved MAP65/PRC1/Ase1 family drastically decrease MT rigidity. Their MT-binding domain mediates this effect. Remarkably, the softening effect of MAP65 observed on single MTs is maintained when MTs are cross-linked. By reconstituting physical collisions between growing MTs/MT bundles, we further show that the decrease in MT stiffness induced by MAP65 proteins is responsible for the sharp bending deformations observed in cells when they coalign at a steep angle to create bundles. Taken together, these data provide new insights into how MAP65, by modifying MT mechanical properties, may regulate the formation of complex MT arrays.
微管(MTs)是参与众多细胞过程的动态细胞骨架元件。尽管它们是具有 1-8 毫米的持久长度的高度刚性聚合物,但它们在细胞内的几微米范围内可能呈现弯曲形状,这取决于它们的生物学功能。然而,细胞中 MT 弯曲刚性如何受到调节仍知之甚少。在这里,我们询问 MAP 是否可以局部控制 MT 的力学性质。我们表明,保守的 MAP65/PRC1/Ase1 家族的两个主要交联剂极大地降低了 MT 的刚性。它们的 MT 结合域介导了这种效应。值得注意的是,当 MT 交联时,在单个 MT 上观察到的 MAP65 软化效应得以维持。通过重新构建生长中的 MT/MT 束之间的物理碰撞,我们进一步表明,MAP65 蛋白诱导的 MT 刚度降低是导致细胞在以陡峭角度共对准以形成束时观察到的急剧弯曲变形的原因。总之,这些数据为 MAP65 通过改变 MT 力学性质来调节复杂 MT 阵列的形成提供了新的见解。