Induction and expression of PGPR-mediated induced resistance against pathogens
Publication date
1998
Authors
Loon, L.C. van
Bakker, P.A.H.M.
Pieterse, C.M.J.
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Document Type
Article in proceedings
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Abstract
Treatment of plants with selected strains of plant growth-promoting rhizobacteria (PGPR) can induce systemic resistance in carnation, cucumber, radish, tobacco, and Arabidopsis as evidenced by an enhanced defensive capacity upon challenge inoculation with a pathogen. In the induction of resistance by Pseudomonas spp. in carnation, radish, and Arabidopsis, the O-antigenic side chain of the bacterial outer membrane lipopolysaccharide acts as an inducing determinant, but other bacterial traits are also involved. Siderophores have been implicated in the induction of resistance in tobacco and Arabidopsis, and a novel type of sideophore, fluorebactin, may explain induction of resistance associated with salicylic acid (SA) in radish. Although some bacterial strains are equally effective in inducing resistance in different plant species, others show specificity which suggests specific recognition between bacteria and plants at the root surface. Moreover, genetic variation for inducibility by specific PGPR strains is present in carnation and Arabidopsis. In contrast to the phenotypically similar systemic acquired resistance (SAR) induced by pathogens, PGPR-mediated induced systemic resistance (ISR) does not always require SA. SAR-associated SA production induces pathogenesis-related proteins (PRs), but no accumulation of PRs was detectable in radish and Arabidopsis expressing ISR. In addition, ISR is fully expressed in Arabidopsis plants transformed with the NahG gene and unable to accumulate SA. In contrast, Arabidopsis mutated in the Etrl gene and insensitive to ethylene, or in the jarl gene and insensitive to jasmonic acid, were no longer inducible. These results demonstrate that compared to pathogens inducing SAR, non-pathogenic rhizobacteria inducing ISR trigger a different signal-transduction pathway not dependent on the accumulation of SA and activation of PR-genes, but dependent on perception of ethylene and jasmonic acid.