SPR2 protects minus ends to promote severing and reorientation of plant cortical microtubule arrays.
SPR2 protects minus ends to promote severing and reorientation of plant cortical microtubule arrays.
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DOI：
10.1083/jcb.201708130
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发表时间：
2018-03-05
期刊：
影响因子：
--
通讯作者：
Ehrhardt DW
中科院分区：
文献类型：
--
作者：
Nakamura M;Lindeboom JJ;Saltini M;Mulder BM;Ehrhardt DW
植物皮层微管阵列的特点是两端都是动态的，但负端是如何控制的还不清楚。中村等人表明，SPR 2动态跟踪并稳定拟南芥微管负末端，调节其切断潜力并响应光感知重新定向皮质阵列。高等植物的皮层微管阵列是在没有中心体的情况下组织起来的，并且具有两端动态的研磨聚合物。聚合物末端稳定性的控制是细胞骨架阵列的组装和组织的基础，但相对较少的是了解如何微管负端控制acentrosomal微管阵列，并没有因素已被确定在高等植物中的cross-milling负端的行为。在这里，我们确定拟南芥SPIRAL 2（SPR 2）作为一种蛋白质，跟踪负端，并保护他们免受亚基损失。SPR 2的功能是促进植物皮层阵列的快速重定向所需的光感知刺激，这是一个过程，是由微管切断，以创建一个新的微管群体驱动。定量活细胞成像和计算机模拟显示，SPR 2的负保护作用通过一种意想不到的机制来促进潜在SPR 2切断位点的寿命，增加切断的可能性，从而快速扩增新的微管阵列。
Cortical microtubule arrays of plants feature treadmilling polymers that are dynamic at both ends, but how the minus ends are controlled is unclear. Nakamura et al. show that SPR2 dynamically tracks and stabilizes microtubule minus ends in Arabidopsis thaliana, which regulates their severing potential and reorients cortical arrays in response to light perception. The cortical microtubule arrays of higher plants are organized without centrosomes and feature treadmilling polymers that are dynamic at both ends. The control of polymer end stability is fundamental for the assembly and organization of cytoskeletal arrays, yet relatively little is understood about how microtubule minus ends are controlled in acentrosomal microtubule arrays, and no factors have been identified that act at the treadmilling minus ends in higher plants. Here, we identify Arabidopsis thaliana SPIRAL2 (SPR2) as a protein that tracks minus ends and protects them against subunit loss. SPR2 function is required to facilitate the rapid reorientation of plant cortical arrays as stimulated by light perception, a process that is driven by microtubule severing to create a new population of microtubules. Quantitative live-cell imaging and computer simulations reveal that minus protection by SPR2 acts by an unexpected mechanism to promote the lifetime of potential SPR2 severing sites, increasing the likelihood of severing and thus the rapid amplification of the new microtubule array.
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