Roles of the reactive oxygen species-generating peroxidase reactions in plant defense and growth induction

TLDR: A novel model for IAA signaling pathway mediated by extracellular ROS produced by cell-wall POXs is proposed and possible controls of the IAA-POX reactions by a fungal alkaloid are discussed.

Abstract: Extracellularly secreted plant peroxidases (POXs) are considered to catalyze the generation of reactive oxygen species (ROS) coupled to oxidation of plant hormone indole-3-acetic acid (IAA) and defense-related compounds salicylic acid (SA), aromatic monoamines (AMAs) and chitooligosaccharides (COSs). This review article consists of two parts, which describe H2O2-dependent and H2O2-independent mechanisms for ROS generation, respectively. Recent studies have shown that plant POXs oxidize SA, AMAs and COSs in the presence of H2O2 via a conventional POX cycle, yielding the corresponding radical species, such as SA free radicals. These radical species may react with oxygen, and superoxide (O2·−) is produced. Through the series of reactions 2 moles of O2·− can be formed from 1 moles of H2O2, thus leading to oxidative burst. It has been revealed that the ROS induced by SA, AMAs and COSs triggers the increase in cytosolic Ca2+ concentration. Actually POXs transduce the extracellular signals into the redox signals that eventually stimulate the intracellular Ca2+ signaling required for induction of defense responses. On the other hand, IAA can react with oxygen and plant POXs in the absence of H2O2, by forming the ternary complex enzyme-IAA-O2, which readily dissociates into enzyme, IAA radicals and O2·−. This article covers the recent reports showing that extracellularly produced hydroxy radicals derived from O2·− mediate the IAA-induced cell elongation. Here a novel model for IAA signaling pathway mediated by extracellular ROS produced by cell-wall POXs is proposed. In addition, possible controls of the IAA-POX reactions by a fungal alkaloid are discussed.