State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China.
State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
Curr Biol. 2018 Apr 23;28(8):1311-1317.e3. doi: 10.1016/j.cub.2018.03.007. Epub 2018 Apr 12.
Plant cells do not possess centrosomes, which serve as the microtubule organizing center in animal cells; how plant cell microtubule arrays are established and maintain their dynamics remain poorly understood [1]. The γ-tubulin complex and the katanin complex play central roles in the organization of plant cortical microtubules [2-6]. Previously, we reported that the augmin complex recruits the γ-tubulin complex to preexisting microtubules and initiates microtubule nucleation [7]. Moreover, we described how an intricate interaction between the katanin p60 subunit KTN1 and the p80 subunit KTN80 confers precise microtubule severing at either microtubule branching nucleation sites or crossovers [8]. Here, we observed that augmin preferentially localizes to microtubule crossovers. Live-cell observations and analyses revealed that, whereas a small portion of crossover-localized augmin complexes act to trigger nascent microtubule nucleation, the majority function in stabilizing the architecture of microtubule crossovers. Finally, genetic analyses and computational modeling confirmed that suppression of augmin activity elevates microtubule severing frequency and facilitates the formation of aligned microtubule arrays. Combined, our findings reveal an unexpected role of augmin and demonstrate that augmin antagonizes katanin-mediated microtubule severing. Furthermore, we propose a novel mechanism for how augmin determines self-organization of plant cortical microtubules by preventing microtubule severing at crossovers in addition to triggering microtubule nucleation.
植物细胞不具有中心体，中心体是动物细胞中微管组织中心；植物细胞微管阵列如何建立以及如何维持其动态性仍然知之甚少[1]。γ-微管蛋白复合物和katanin 复合物在植物皮层微管的组织中起核心作用[2-6]。以前，我们报道过augmin 复合物将γ-微管蛋白复合物募集到预先存在的微管上，并启动微管核形成[7]。此外，我们描述了katanin p60 亚基 KTN1 和 p80 亚基 KTN80 之间复杂的相互作用如何在微管分支核形成位点或交叉处精确地进行微管切割[8]。在这里，我们观察到 augmin 优先定位于微管交叉处。活细胞观察和分析表明，虽然一小部分交叉定位的 augmin 复合物作用于触发新的微管核形成，但大多数复合物的功能在于稳定微管交叉的结构。最后，遗传分析和计算建模证实，抑制 augmin 活性会增加微管切割的频率，并促进对齐的微管阵列的形成。综上所述，我们的研究结果揭示了 augmin 的一个意想不到的作用，并表明 augmin 拮抗了katanin 介导的微管切割。此外，我们提出了一个新的机制，说明了 augmin 如何通过防止微管在交叉处切割来决定植物皮层微管的自我组织，除了触发微管核形成之外。
