High-order mutants reveal an essential requirement for peroxidases but not laccases in Casparian strip lignification

第一作者：Nelson Rojas-Murcia

第一单位：瑞士洛桑大学

通讯作者：Niko Geldner

 Abstract 

背景回顾：Lignin has enabled plants to colonize land, grow tall, transport water within their bodies, and protect themselves against various stresses. Consequently, this polyphenolic polymer, impregnating cellulosic plant cell walls, is the second most abundant polymer on Earth.

提出问题：Yet, despite its great physiological, ecological, and economical importance, our knowledge of lignin biosynthesis in vivo, especially the polymerization steps within the cell wall, remains vague—specifically, the respective roles of the two polymerizing enzymes classes, laccases and peroxidases.

关键难点：One reason for this lies in the very high numbers of laccases and peroxidases encoded by 17 and 73 homologous genes, respectively, in Arabidopsis.

研究对象：Here, we have focused on a specific lignin structure, the ring-like Casparian strips (CSs) within the root endodermis.

结果1-漆酶：By reducing candidate numbers using cellular resolution expression and localization data and by boosting stacking of mutants using CRISPR-Cas9, we mutated the majority of laccases in Arabidopsis in a nonuple mutant—essentially abolishing laccases with detectable endodermal expression. Yet, we were unable to detect even slight defects in CS formation.

结果2-过氧化物酶：By contrast, we were able to induce a complete absence of CS formation in a quintuple peroxidase mutant.

结论：Our findings are in stark contrast to the strong requirement of xylem vessels for laccase action and indicate that lignin in different cell types can be polymerized in very distinct ways.

推测：We speculate that cells lignify differently depending on whether lignin is localized or ubiquitous and whether cells stay alive during and after lignification, as well as the composition of the cell wall.

 通讯作者 

doi: 10.1073/pnas.2012728117

Journal: PNAS

First Published: Nov 02, 2020

p.s. 通讯往期精彩链接：

The EMBO Journal：拟南芥根组织单个细胞损伤诱导乙烯响应通路