The cell cycle controls spindle architecture in Arabidopsis by modulating the augmin pathway

Mariana Romeiro Motta, Francois Nedelec, Elke Woelken, Helen Saville, Claire Jacquerie, Martine Pastuglia, Sara Christina Stolze, Eveline Van De Slijke, Poyu Chen, Lev Boettger, Katia Belcram, Hirofumi Nakagami, Geert De Jaeger, David Bouchez, Arp Schnittger
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Abstract

To ensure an even segregation of chromosomes during somatic cell division, eukaryotes rely on specific microtubule structures called mitotic spindles. There are, however, striking differences in overall spindle organization among eukaryotic super groups, and in particular little is known about how spindle architecture is determined in plants. As a foundation for our work, we have measured prime characteristics of Arabidopsis mitotic spindles and built a three-dimensional dynamic model of the Arabidopsis mitotic spindle using Cytosim. Next, we identified the cell-cycle regulator CYCLIN-DEPENDENT KINASE B1 (CDKB1) together with its cyclin partner CYCB3;1 as key regulators of spindle shape and organization in Arabidopsis. Loss of CDKB1 function resulted in a high number of astral microtubules that are normally absent from plant spindles, as opposed to animal ones. We identified an augmin complex member, ENDOSPERM DEFECTIVE1 (EDE1), as a substrate of the CDKB1;1-CYCB3;1 complex. A non-phosphorylatable mutant of EDE1 displayed spindles with extended pole-to-pole distance, resembling the phenotypes of cycb3;1 and cdkb1 mutants. Moreover, we found that the mutated EDE1 version associated less efficiently with spindle microtubules. Consistently, reducing the level of augmin in Cytosim simulations largely recapitulated the spindle phenotypes observed in cycb3;1 and cdkb1 mutants. Our results emphasize the importance of cell cycle-dependent phospho-control of the mitotic spindle in plant cells. They also support the validity of our computational model as a framework for the exploration of mechanisms controlling the organization of the spindle in plants and in other species.
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细胞周期通过调节augmin通路控制拟南芥的纺锤体结构
为了确保体细胞分裂过程中染色体的均匀分离,真核生物依赖于称为有丝分裂纺锤体的特定微管结构。然而,真核超群中纺锤体的整体结构存在显著差异,特别是关于植物中纺锤体结构是如何确定的知之甚少。作为本研究的基础,我们测量了拟南芥有丝分裂纺锤体的基本特征,并利用Cytosim建立了拟南芥有丝分裂纺锤体的三维动态模型。接下来,我们确定了细胞周期调节因子cyclin - dependent KINASE B1 (CDKB1)及其周期蛋白伙伴CYCB3;1是拟南芥纺锤体形状和组织的关键调节因子。CDKB1功能的缺失导致植物纺锤体中大量星体微管的缺失,而动物纺锤体中通常没有星体微管。我们发现了一个augmin复合物成员,ENDOSPERM DEFECTIVE1 (EDE1),作为CDKB1 - cycb3 - 1复合物的底物。EDE1的非磷酸化突变体显示出具有延长的极对极距离的纺锤体,类似于cycb3;1和cdkb1突变体的表型。此外,我们发现突变的EDE1版本与纺锤体微管的关联效率较低。一致地,在Cytosim模拟中降低augmin水平在很大程度上再现了在cycb3;1和cdkb1突变体中观察到的纺锤体表型。我们的研究结果强调了植物细胞有丝分裂纺锤体的细胞周期依赖性磷酸化控制的重要性。它们还支持我们的计算模型作为探索控制植物和其他物种纺锤体组织机制的框架的有效性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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