Evidence for the Involvement of an Oxidative Stress in the Initiation of Infection of Pear by Erwinia amylovora  

Abstract

Involvement of an oxidative burst, usually related to incompatible plant/pathogen interactions leading to hypersensitive reactions, was investigated with Erwinia amylovora, the causal agent of fire blight of Maloideae subfamily of Rosaceae, in interaction with pear (Pyrus communis; compatible situation) and tobacco (Nicotiana tabacum; incompatible situation). As expected, this necrogenic bacterium induced in tobacco a sustained production of superoxide anion, lipid peroxidation, electrolyte leakage, and concomitant increases of several antioxidative enzymes (ascorbate peroxidases, glutathion reductases, glutathion-S-transferases, and peroxidases), in contrast to the compatible pathogen Pseudomonas syringae pv tabaci, which did not cause such reactions. In pear leaves, however, inoculations with both the disease-and the hypersensitive reaction-inducing bacteria (E. amylovora and P. syringae pv tabaci, respectively) resulted in superoxide accumulation, lipid peroxidation, electrolyte leakage, and enzyme induction at similar rates and according to equivalent time courses. The unexpected ability of E. amylovora to generate an oxidative stress even in compatible situation was linked to its functional hrp (for hypersensitive reaction and pathogenicity) cluster because an Hrp secretion mutant of the bacteria did not induce any plant response. It is suggested that E. amylovora uses the production of reactive oxygen species as a tool to provoke host cell death during pathogenesis to invade plant tissues. The bacterial exopolysaccharide could protect this pathogen against the toxic effects of oxygen species since a non-capsular mutant of E. amylovora induced locally the same responses than the wild type but was unable to further colonize the plant.

Phenolic profiles in apple leaves and the efficacy of selected phenols against fire blight (Erwinia amylovora)

“…The antioxidative activity of phenolics can contribute to plant resistance during the oxidative burst and the HR (Venisse et al 2001;Gosch et al 2010). Dugé de Bernonville et al (2011) provided evidence for bioactivity of dihydrochalcones -especially phloridzin -as functional antioxidants.…”

“…In similarity to other plant-pathogen interactions, the first line of host defense against fire blight is accompanied with oxidative burst, lipid peroxidation, shift in ion fluxes and induction of local reactions such as the hypersensitive response (HR) (Venisse et al 2001;Iakimova et al 2013). Accumulation of phytoalexins, activation of pathogenesis-related proteins and modification of plant hormone balance are often observed (Bonasera et al 2006;Dugé de Bernonville et al 2012; Van der Zwet et al 2012).…”

Molecular Characterization of Natural Erwinia pyrifoliae Strains Deficient in Hypersensitive Response

“…Although Ep2/97 was not virulent due to its inability to damage plant cells, the wild-type strain relieved the restriction, allowing both strains to grow. In the presence of wild-type cells, a spontaneous HR-deficient variant may be advantageous in pear tissue, because it does not challenge the plant defense mechanism (18). In addition, the variant could also have a better chance than the HR-positive parent strain for survival during decline of the population in a late stage of plant colonization.…”

Involvement of coronatine-inducible reactive oxygen species in bacterial speck disease of tomato

“…10 ROS functions in the stimulation of hypersensitive cell death 11,12 and disease-associated necrotic cell death. 13,14 The signals associated with plant innate immunity include ion flux, the oxidative burst, activation of MAP kinase cascades, and defense gene expression; these responses are triggered by the perception of pathogen-associated molecular patterns (PAMPs). 15 Thus, during the early stages of infection, Pst DC3000 might use several effectors or virulence factors to suppress PAMP-inducible ROS and the resulting PAMPtriggered immunity (PTI).…”