Abstract

We studied changes in gas exchange, photochemical activity and the antioxidant system in cucumber leaves locally infected with Pseudomonas syringae pv lachrymans and in uninfected systemic ones. Infection-induced declined net photosynthesis rate and the related changes in transpiration rate, the intracellular CO2 concentration, and prolonged reduction in maximal PSII quantum yield (Fv/Fm), accompanied by an increase in non-photochemical quenching (NPQ), were observed only in the infected leaves, along with full disease symptom development. Infection severely affected the ROS/redox homeostasis at the cellular level and in chloroplasts. Superoxide dismutase, ascorbate, and tocopherol were preferentially induced at the early stage of pathogenesis, whereas catalase, glutathione, and the ascorbate–glutathione cycle enzymes were activated later. Systemic leaves retained their net photosynthesis rate and the changes in the antioxidant system were partly like those in the infected leaves, although they occurred later and were less intense. Re-balancing of ascorbate and glutathione in systemic leaves generated a specific redox signature in chloroplasts. We suggest that it could be a regulatory element playing a role in integrating photosynthesis and redox regulation of stress, aimed at increasing the defense capacity and maintaining the growth of the infected plant.

Highlights

  • Reactive oxygen species (ROS) and redox signaling play multiple roles in plant biology by mediating metabolic, growth and developmental processes as well as plant response to stress [1,2,3]

  • We suggest that the changes in the ascorbateand glutathione-related redox signature in the systemic leaves induced by local bacterial infection, linked to the modified photochemical activity, could represent redox homeostasis mAintaining mechanism which allows controlling gene expression and metabolic activities, supporting the defensive capacity and growth of the infected plant

  • The pathogen-induced decline in photochemical activity and net photosynthesis rate was restricted to the infected leaves whereas the systemic ones retained their photosynthetic capacity for potential activating acclimation and defense mechanisms

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Summary

Introduction

Reactive oxygen species (ROS) and redox signaling play multiple roles in plant biology by mediating metabolic, growth and developmental processes as well as plant response to stress [1,2,3]. Most environmental stressors, including pathogens, disturb the cellular redox environment which is buffered by the mAin soluble redox couples, i.e., reduced and oxidized ascorbate (AA/DHA), reduced and oxidized glutathione (GSH/GSSG) as well as reduced and oxidized nicotinamide adenine dinucleotide phosphate (NADPH/NADP). The redox homeostasis is largely influenced by ROS, including those generated during photosynthesis and other metabolic processes, which are overproduced under stress conditions. Rapid generation of ROS, mAinly superoxide anion radical (O2−) and H2O2, is one of the earliest plant responses to pathogens observed in numerous plant–pathogen interactions [5,6,7]. Among ROS, H2O2 which is a relatively stable and non-charged molecule, is considered a versatile signaling molecule involved in the intracellular communication system that activates stress responses, including redox-dependent reprogramming of defense gene expression [8,9]

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