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拟南芥绒毛蛋白2和绒毛蛋白3通过肌动蛋白丝的捆绑在厚壁组织发育中发挥冗余作用。

Arabidopsis VILLIN2 and VILLIN3 act redundantly in sclerenchyma development via bundling of actin filaments.

作者信息

Bao Chanchan, Wang Juan, Zhang Ruihui, Zhang Baocai, Zhang Hua, Zhou Yihua, Huang Shanjin

机构信息

Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.

出版信息

Plant J. 2012 Sep;71(6):962-75. doi: 10.1111/j.1365-313X.2012.05044.x. Epub 2012 Jun 28.

DOI:10.1111/j.1365-313X.2012.05044.x
PMID:22563899
Abstract

The organization of the actin cytoskeleton has been implicated in sclerenchyma development. However, the molecular mechanisms linking the actin cytoskeleton to this process remain poorly understood. In particular, there have been no studies showing that direct genetic manipulation of the actin cytoskeleton affects sclerenchyma development. Villins belong to the villin/gelsolin/fragmin superfamily and are versatile actin-modifying proteins. Several recent studies have implicated villins in tip growth of single cells, but how villins act in multicellular plant development remains largely unknown. Here, we found that two closely related villin isovariants from Arabidopsis, VLN2 and VLN3, act redundantly in sclerenchyma development. Detailed analysis of cross-sections from inflorescence stems of vln2 vln3 double mutant plants revealed a reduction in stem size and in the number of vascular bundles; however, no defects in synthesis of the secondary cell wall were detected. Surprisingly, the vln2 vln3 double mutation did not affect cell elongation of inter-fascicular fibers. Biochemical analyses showed that recombinant VLN2 was able to cap, sever and bundle actin filaments, similar to VLN3. Consistent with these biochemical activities, loss of function of VLN2 and VLN3 resulted in a decrease in the amount of F-actin and actin bundles in plant cells. Collectively, our findings demonstrate that VLN2 and VLN3 act redundantly in sclerenchyma development via bundling of actin filaments.

摘要

肌动蛋白细胞骨架的组织与厚壁组织的发育有关。然而,将肌动蛋白细胞骨架与这一过程联系起来的分子机制仍知之甚少。特别是,尚无研究表明对肌动蛋白细胞骨架进行直接基因操作会影响厚壁组织的发育。维林蛋白属于维林蛋白/凝溶胶蛋白/肌动蛋白片段化蛋白超家族,是多功能的肌动蛋白修饰蛋白。最近的几项研究表明维林蛋白参与单细胞的顶端生长,但维林蛋白在多细胞植物发育中的作用仍 largely 未知。在这里,我们发现拟南芥中两个密切相关的维林蛋白同工型 VLN2 和 VLN3 在厚壁组织发育中起冗余作用。对 vln2 vln3 双突变体植物花序茎横切面的详细分析表明,茎的大小和维管束数量减少;然而,未检测到次生细胞壁合成的缺陷。令人惊讶的是,vln2 vln3 双突变并不影响束间纤维的细胞伸长。生化分析表明,重组 VLN2 能够帽化、切断和捆绑肌动蛋白丝,与 VLN3 类似。与这些生化活性一致,VLN2 和 VLN3 的功能丧失导致植物细胞中 F-肌动蛋白和肌动蛋白束的数量减少。总的来说,我们的研究结果表明,VLN2 和 VLN3 通过捆绑肌动蛋白丝在厚壁组织发育中起冗余作用。

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