Abstract
Ethylene interacts with other plant hormones to modulate many aspects of plant metabolism, including defence and stomata regulation. Therefore, its manipulation may allow plant pathogens to overcome the host’s immune responses. This work investigates the role of ethylene as a virulence factor for Pseudomonas syringae pv. actinidiae (Psa), the aetiological agent of the bacterial canker of kiwifruit. The pandemic, highly virulent biovar of this pathogen produces ethylene, whereas the biovars isolated in Japan and Korea do not. Ethylene production is modulated in planta by light/dark cycle. Exogenous ethylene application stimulates bacterial virulence, and restricts or increases host colonisation if performed before or after inoculation, respectively. The deletion of a gene, unrelated to known bacterial biosynthetic pathways and putatively encoding for an oxidoreductase, abolishes ethylene production and reduces the pathogen growth rate in planta. Ethylene production by Psa may be a recently and independently evolved virulence trait in the arms race against the host. Plant- and pathogen-derived ethylene may concur in the activation/suppression of immune responses, in the chemotaxis toward a suitable entry point, or in the endophytic colonisation.
Highlights
The key steps in pathogen recognition and plant defence activation are strictly controlled by hormonal signals [1,2]
Among the Psa strains tested in this experiment, only those belonging to biovar 3 (CFBP7286, 10,787 and Arg2.1) showed a detectable ethylene release when grown on fresh plant extract (FPE) (Figure 1)
Ethylene production by P. syringae pv. glycinea, that was used as positive control, was two orders of magnitude higher than by any Psa strain
Summary
The key steps in pathogen recognition and plant defence activation are strictly controlled by hormonal signals [1,2]. More specific defences are triggered by salicylic acid (SA)-, ethylene- and jasmonic acid (JA)-dependent signalling pathways. SA elicits responses against biotrophic pathogens, while ethylene/JA-mediated defences are activated against necrotrophs. Due to the opposite lifestyles of their target pathogens, it is generally recognised that SA and ethylene/JA signalling pathways are mutually antagonistic [2]. This basic model is complicated by the existence of many points of interaction among the signal cascades. For instance, is induced by SA [4,5] in the early stages of the infection, but contributes to SA signal suppression in its subsequent interplay with JA [1]
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