National Key Laboratory of Plant Molecular Genetics and Chinese Academy of Sciences Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China, and University of the Chinese Academy of Sciences, Beijing, 100049, China.
National Key Laboratory of Plant Molecular Genetics and Chinese Academy of Sciences Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China, and University of the Chinese Academy of Sciences, Beijing, 100049, China
Plant Physiol. 2018 Jun;177(2):671-683. doi: 10.1104/pp.17.01279. Epub 2018 Apr 20.
During the growth and development of land plants, some specialized cells, such as tracheary elements, undergo secondary cell wall thickening. Secondary cell walls contain additional lignin, compared with primary cell walls, thus providing mechanical strength and potentially improving defenses against pathogens. However, the molecular mechanisms that initiate wall thickening are unknown. In this study, we identified an Arabidopsis () leucine-rich repeat receptor-like kinase, encoded by (), that is expressed specifically in cells undergoing secondary cell wall thickening. Suppression of expression resulted in a range of phenotypes that included retarded early elongation of the inflorescence stem, shorter fibers, slower root growth, and shorter flower filaments. In contrast, up-regulation of led to longer fiber cells, reduced secondary cell wall thickening in fiber and vessel cells, and defects in anther dehiscence. Molecular and cellular analyses showed that down-regulation of promoted secondary cell wall thickening and up-regulation of enhanced cell elongation and inhibited secondary cell wall thickening. We propose that AtVRLK1 functions as a signaling component in coordinating cell elongation and cell wall thickening during growth and development.
在陆生植物的生长和发育过程中,一些特化细胞,如导管分子,经历次生细胞壁的加厚。与初生细胞壁相比,次生细胞壁含有额外的木质素,从而提供机械强度,并可能提高对病原体的防御能力。然而,启动细胞壁加厚的分子机制尚不清楚。在这项研究中,我们鉴定了一个拟南芥(Arabidopsis)富含亮氨酸重复受体样激酶,由 ()编码,该激酶在经历次生细胞壁增厚的细胞中特异性表达。 表达的抑制导致一系列表型,包括花序茎早期伸长迟缓、纤维变短、根生长缓慢和花丝变短。相比之下, 的上调导致纤维细胞变长,纤维和导管细胞的次生细胞壁加厚减少,以及花药开裂缺陷。分子和细胞分析表明, 的下调促进次生细胞壁加厚,而上调 增强细胞伸长并抑制次生细胞壁加厚。我们提出,AtVRLK1 作为一个信号组成部分,在生长和发育过程中协调细胞伸长和细胞壁加厚。