RBOH1-dependent apoplastic H2O2 mediates epigallocatechin-3-gallate-induced abiotic stress tolerance in Solanum lycopersicum L.

Abstract

Responses of plants to abiotic stimuli are mediated by a plethora of bioactive compounds. Flavonoids are a large group of plant secondary metabolites, playing diverse roles in plant growth, development and responses to stress. Despite the recent report on epigallocatechin-3-gallate (EGCG, a bioactive flavonoids)-induced enhanced tolerance to salt stress, the underlying molecular mechanisms of stress tolerance remain unclear. Moreover, whether such stress protective role of EGCG is common for other environmental stressors also remains elusive. In the current study, we showed that EGCG functions as a broad spectrum stress protectant that alleviates a variety of abiotic stresses such as cold, heat, salinity and drought in tomato plants. While those abiotic stresses inhibited leaf photosynthetic activity by enhancing reactive oxygen species (ROS) production and membrane damage, exogenous EGCG protected photosynthetic apparatus by reducing ROS accumulation. Furthermore, EGCG-induced attenuation of ROS accumulation was largely attributed to the enhanced activity of antioxidant enzymes such as superoxide dismutase (SOD), peroxidase (POD), catalase (CAT) and ascorbate peroxidase (APX). Analysis of sub-cellular localization of ROS revealed that EGCG preferentially induced apoplastic H2O2 production by activation of RESPIRATORY BURST OXIDASE HOMOLOG1 (RBOH1)-encoded NADPH oxidase. Further investigation using virus-induced gene silencing showed that suppression of RBOH1 expression aggravated abiotic stress-induced ROS accumulation and compromised EGCG-induced ROS scavenging, implying that RBOH1-dependent H2O2 production is critical for the EGCG-induced tolerance to abiotic stress. This study advances our current understanding of stress protective role of flavonoids and unveils a critical mechanism of EGCG-induced abiotic stress tolerance in tomato plants.