Abstract

Citrus bacterial canker (CBC) results from Xanthomonas citri subsp. citri (Xcc) infection and poses a grave threat to citrus production. Class III peroxidases (CIII Prxs) are key proteins to the environmental adaptation of citrus plants to a range of exogenous pathogens, but the role of CIII Prxs during plant resistance to CBC is poorly defined. Herein, we explored the role of CsPrx25 and its contribution to plant defenses in molecular detail. Based on the expression analysis, CsPrx25 was identified as an apoplast-localized protein that is differentially regulated by Xcc infection, salicylic acid, and methyl jasmone acid in the CBC-susceptible variety Wanjincheng (C. sinensis) and the CBC-resistant variety Calamondin (C. madurensis). Transgenic Wanjincheng plants overexpressing CsPrx25 were generated, and these transgenic plants exhibited significantly increased CBC resistance compared with the WT plants. In addition, the CsPrx25-overexpressing plants displayed altered reactive oxygen species (ROS) homeostasis accompanied by enhanced H2O2 levels, which led to stronger hypersensitivity responses during Xcc infection. Moreover, the overexpression of CsPrx25 enhanced lignification as an apoplastic barrier for Xcc infection. Taken together, the results highlight how CsPrx25-mediated ROS homeostasis reconstruction and cell wall lignification can enhance the resistance of sweet orange to CBC.

Highlights

  • Plants possess an intricate repertoire of cell-based defense systems to maintain their resistance to potentially harmful pathogens[1,2]

  • The primary sequences were searched in PeroxiScan, which is built in RedoxiBase[44,45]

  • CIII Prxs belong to a plant-specific multigene family that promotes disease resistance[18,33,34], lignification, the flexibility of cell walls and suberization[29,30]

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Summary

Introduction

Plants possess an intricate repertoire of cell-based defense systems to maintain their resistance to potentially harmful pathogens[1,2]. As an immediate pathogen recognition response, oxidative bursts produced in apoplasts induce reactive oxygen species (ROS), including superoxide (O2.−) and H2O2, as a first line of defense[3]. The current models of plant responses include ROS and other radicals as catalysts of covalent cell-wall modifications[4], as signals for cell-death reactions[5,6] and as regulators of resistance-associated genes[7,8]. Antioxidant enzyme activities and ROS homeostasis are regulated by important plant hormones, including jasmonic acid (JA) and salicylic acid (SA)[15,16,17]

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