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The receptor-like kinase AtVRLK1 regulates secondary cell wall thickening
First author: Cheng Huang; Affiliations: Institute of Plant Physiology and Ecology, Chinese Academy of Sciences (中科院植物生理生态研究所): Shanghai, China
Corresponding author: Laigeng Li
During the growth and development of land plants, some specialized cells, such as tracheary elements (导管分子), 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 thalianaleucine-rich repeat receptor-like kinase, encoded by AtVRLK1(Vascular-Related RLK 1), that is specifically expressed in cells undergoing secondary cell wall thickening. Suppression of AtVRLK1expression resulted in a range of phenotypes that included retarded (减速) early elongation of the inflorescence stem, shorter fibers, slower root growth, and shorter flower filaments (花丝). In contrast, upregulation of AtVRLK1led to longer fiber cells, reduced secondary cell wall thickening in fiber and vessel cells, and defects in anther dehiscence (花药开裂). Molecular and cellular analyses showed that downregulation of AtVRLK1promoted secondary cell wall thickening and upregulation of AtVRLK1enhanced 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.
在植物的生长和发育过程中,诸如导管分子等一些特异的细胞会经历次生细胞壁加厚过程。相比于初生细胞壁,次生细胞壁具有额外的木质素,这会导致机械强度增加,并潜在提升对于病原菌的抗性。然而,目前对于次生细胞壁加厚的起始机理还不清楚。本文鉴定了一个拟南芥亮氨酸重复类受体激酶AtVRLK1基因,其特异在经历次生细胞壁加厚的细胞中表达。抑制AtVRLK1基因的表达会导致诸多表型的变化,比如花序轴早期伸长减缓、纤维变短、根生长减缓、花丝长度变短。相反,上调AtVRLK1基因的表达则会导致纤维细胞增长,纤维和维管细胞中次生细胞壁加厚减少,并且花药开裂存在缺陷。分子和细胞学试验显示下调AtVRLK1基因的表达会促进次生细胞壁加厚,而上调AtVRLK1基因的表达会增强细胞伸长和起始次生细胞壁加厚。作者提出AtVRLK1可能作为植物生长发育过程中调控细胞伸长和细胞壁加厚之间平衡的信号组份。