The Key Roles of ROS and RNS as a Signaling Molecule in Plant-Microbe Interactions

Abstract

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play a pivotal role in the dynamic cell signaling systems in plants, even under biotic and abiotic stress conditions. Over the past two decades, various studies have endorsed the notion that these molecules can act as intracellular and intercellular signaling molecules at a very low concentration to control plant growth and development, symbiotic association, and defense mechanisms in response to biotic and abiotic stress conditions. However, the upsurge of ROS and RNS under stressful conditions can lead to cell damage, retarded growth, and delayed development of plants. As signaling molecules, ROS and RNS have gained great attention from plant scientists and have been studied under different developmental stages of plants. However, the role of RNS and RNS signaling in plant-microbe interactions is still unknown. Different organelles of plant cells contain the enzymes necessary for the formation of ROS and RNS as well as their scavengers, and the spatial and temporal positions of these enzymes determine the signaling pathways. In the present review, we aimed to report the production of ROS and RNS, their role as signaling molecules during plant-microbe interactions, and the antioxidant system as a balancing system in the synthesis and elimination of these species.

Keywords: RNS; ROS; antioxidant system; plant–microbe interactions; signaling.

Figure 1

(A) All types of reactive oxygen species (ROS) in plants and (B) sites of ROS production in the plant cell.

Figure 2

Schematic representation of ROS in PTI, ETI, and symbiotic association.

Figure 3

(A) All types of reactive nitrogen species (ROS) in plants, (B) oxidative and reductive pathways, (C) sites of NO production.

Figure 4

Proposed model of action for GSNOR and NR in NO homeostasis and plant immunity. After the exposure to the pathogen, activation of NR at the local site leads to accumulation of NO₂⁻, which is reduced to NO by the mitochondrial electron transport system. The new production of NO rapidly increases the concentration of GSNO and other nitrosothiols; moreover, the transcriptional inhibition of GSNOR also contributes to maintaining the enhanced GSNO pool.