Role of electron transport chain of chloroplasts in oxidative burst of interaction between Erwinia amylovora and host cells

Abstract

Erwinia amylovora is a necrogenic bacterium, causing the fire blight disease on many rosaceous plants. Triggering oxidative burst by E. amylovora is a key response by which host plants try to restrain pathogen spread. Electron transport chain (ETC) of chloroplasts is known as an inducible source of reactive oxygen species generation in various stresses. This research was performed to assess the role of this ETC in E. amylovora-host interaction using several inhibitors of this chain in susceptible and resistant apple and pear genotypes. All ETC inhibitors delayed appearance of disease necrosis, but the effects of methyl viologen, glutaraldehyde, and DCMU were more significant. In the absence of inhibitors, resistant genotypes showed an earlier and severe H2O2 generation and early suppression of redox dependent, psbA gene. The effects of inhibitors were corresponding to the redox potential of ETC inhibitory sites. In addition, delayed necrosis appearance was associated with the decreased disease severity and delayed H2O2 generation. These results provide evidences for the involvement of this ETC in host oxidative burst and suggest that chloroplast ETC has significant role in E. amylovora-host interaction.

Chromosomally Encoded hok-sok Toxin-Antitoxin System in the Fire Blight Pathogen Erwinia amylovora: Identification and Functional Characterization

“…Reactive oxygen species, including hydrogen peroxide, are common sources of DNA damage during bacterial stress (57,58), and supplementation with hydrogen peroxide or deletion of catalase genes is a trigger of filamentation in some species (59,60). During infection, E. amylovora must contend with ROS generated by the host defense response (40,(61)(62)(63). Regulation of bacterial catalase activity has been previously shown in the type II TA systems MqsR/MqsA and YafQ/DinJ in E. coli, where the antitoxins MqsA and DinJ both affect bacterial catalase by decreasing the level of RpoS, a positive regulator of katG and katE catalase genes (64)(65)(66).…”

Erwinia amylovora catalases KatA and KatG are virulence factors and delay the starvation‐induced viable but non‐culturable (VBNC) response

“…The E. amylovora life cycle comprises periods during which it needs to overcome oxidative stress. When inside a plant, E. amylovora has to cope with the H 2 O 2 released by host cells, during either compatible or incompatible plant-pathogen interactions (Abdollahi et al, 2015;Venisse et al, 2001Venisse et al, , 2003. During incompatible interactions, E. amylovora cells are detected by plant cells, which respond with an oxidative burst, followed by a hypersensitive response (HR), usually reducing the pathogen populations and stopping tissue colonization (Venisse et al, 2001).…”

“…During incompatible interactions, E. amylovora cells are detected by plant cells, which respond with an oxidative burst, followed by a hypersensitive response (HR), usually reducing the pathogen populations and stopping tissue colonization (Venisse et al, 2001). In compatible interactions, however, although many phytopathogenic bacteria use a type III secretion system (TTSS) to avoid or reduce both the release of ROS and the HR (Berger et al, 2007;Fones and Preston, 2012), E. amylovora uses it to kill plant cells and progress within host tissues, causing the characteristic necrosis of fire blight disease (Abdollahi et al, 2015;Iakimova et al, 2013;Venisse et al, 2001Venisse et al, , 2003. However, the functional roles of catalases during E. amylovora interactions with plants have not yet been explored.…”

Small RNA ArcZ Regulates Oxidative Stress Response Genes and Regulons in Erwinia amylovora

“…This suggests that during infection E. amylovora may be releasing or actively secreting catalase to reduce damage done to cellular structures when peroxide production is elicited as a part of host-defense responses. In support of the hypothesis that early protection may be important, production of hydrogen peroxide in infected apple and pear shoots occurs early during disease development, as elevated production of hydrogen peroxide occurred ahead of symptom development (Abdollahi et al, 2015). Additionally, because the protein sequence of E. amylovora KatA is more similar to catalases from gram-positive Bacillus subtilis than it is to KatE from E. coli , E. amylovora may have acquired this gene during its evolution as a plant pathogen.…”

“…For example, in tissues with high oxygen availability such as leaves and flowers, E. amylovora cells are interacting with living host cells that are the most prone to mount defense responses including production of reactive oxygen species. It has been shown previously that E. amylovora cells trigger host defense mechanisms including generation of an oxidative burst during compatible interactions (i.e., successful infection) (Venisse et al, 2002, 2003; Iakimova et al, 2013; Abdollahi et al, 2015). Indeed, we demonstrate here that concentrations of hydrogen peroxide in infected apple leaves peak at levels of 4–5 mM at 2 days post-inoculation (Figure 6A).…”