The Receptor-Like Kinase AtVRLK1 Regulates Secondary Cell Wall Thickening
Author(s) -
Cheng Huang,
Rui Zhang,
Jinshan Gui,
Yu Zhong,
Laigeng Li
Publication year - 2018
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.17.01279
Subject(s) - secondary cell wall , thickening , cell wall , microbiology and biotechnology , arabidopsis , elongation , arabidopsis thaliana , cell growth , biology , cell , receptor , biophysics , chemistry , botany , biochemistry , gene , materials science , polymer science , ultimate tensile strength , mutant , metallurgy
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 (Arabidopsis thaliana) leucine-rich repeat receptor-like kinase, encoded by AtVRLK1 (Vascular-Related Receptor-Like Kinase1), that is expressed specifically in cells undergoing secondary cell wall thickening. Suppression of AtVRLK1 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 AtVRLK1 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 AtVRLK1 promoted secondary cell wall thickening and up-regulation of AtVRLK1 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.
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