The Xyloglucan Endotransglucosylase/Hydrolase Gene XTH22/TCH4 Regulates Plant Growth by Disrupting the Cell Wall Homeostasis in Arabidopsis under Boron Deficiency

Abstract

TCH4 is a xyloglucan endotransglucosylase/hydrolase (XTH) family member. Extensive studies have shown that <i>XTHs</i> are very important in cell wall homeostasis for plant growth and development. Boron (B), as an essential micronutrient for plants, plays an essential role in the cross-linking of cell wall pectin. However, the effect of B on cell wall organization is unclear. This study aimed to explore the mechanism of plant adaption to B stress by investigating the role of <i>TCH4</i> in cell wall homeostasis. We conducted both plate and hydroponic cultures of wild-type Col-0 and overexpression and gene knockout lines of <i>XTH22/TCH4</i> to analyze the phenotype, components, and characteristics of the cell wall using immunofluorescence, atomic force microscopy (AFM), and transmission electron microscopy (TEM). B deficiency induces the expression of <i>TCH4</i>. The overexpression lines of <i>TCH4</i> presented more sensitivity to B deficiency than the wild-type Col-0, while the knockout lines of <i>TCH4</i> were more resistant to low B stress. Up-regulation of <i>TCH4</i> influenced the ratio of chelator-soluble pectin to alkali-soluble pectin and decreased the degree of methylesterification of pectin under B-deficient conditions. Moreover, we found that B deficiency disturbed the arrangement of cellulose, enlarged the gap between cellulose microfibrils, and decreased the mechanical strength of the cell wall, leading to the formation of a thickened and deformed triangular region of the cell wall. These symptoms were more profound in the <i>TCH4</i> overexpression lines. Consistently, compared with Col-0, the O₂^- and MDA contents in the <i>TCH4</i> overexpression lines increased under B-deficient conditions. This study identified the B-deficiency-induced <i>TCH4</i> gene, which regulates cell wall homeostasis to influence plant growth under B-deficient conditions.