Abstract
BackgroundInduced resistance is a state of enhanced defensive capacity developed by a plant reacting to specific biotic or chemical stimuli. Over the years, several forms of induced resistance have been characterized, including systemic acquired resistance, which is induced upon localized infection by an avirulent necrotizing pathogen, and induced systemic resistance (ISR), which is elicited by selected strains of nonpathogenic rhizobacteria. However, contrary to the relative wealth of information on inducible defense responses in dicotyledoneous plants, our understanding of the molecular mechanisms underlying induced resistance phenomena in cereal crops is still in its infancy. Using a combined cytomolecular and pharmacological approach, we analyzed the host defense mechanisms associated with the establishment of ISR in rice by the rhizobacterium Serratia plymuthica IC1270.ResultsIn a standardized soil-based assay, root treatment with IC1270 rendered foliar tissues more resistant to the hemibiotrophic pathogen Magnaporthe oryzae, causal agent of the devastating rice blast disease. Analysis of the cytological and biochemical alterations associated with restriction of fungal growth in IC1270-induced plants revealed that IC1270 primes rice for enhanced attacker-induced accumulation of reactive oxygen species (ROS) and autofluorescent phenolic compounds in and near epidermal cells displaying dense cytoplasmic granulation. Similar, yet more abundant, phenotypes of hypersensitively dying cells in the vicinity of fungal hyphae were evident in a gene-for-gene interaction with an avirulent M. oryzae strain, suggesting that IC1270-inducible ISR and R protein conditioned effector-triggered immunity (ETI) target similar defense mechanisms. Yet, this IC1270-inducible ISR response seems to act as a double-edged sword within the rice defense network as induced plants displayed an increased vulnerability to the necrotrophic pathogens Rhizoctonia solani and Cochliobolus miyabeanus. Artificial enhancement of ROS levels in inoculated leaves faithfully mimicked the opposite effects of IC1270 bacteria on aforementioned pathogens, suggesting a central role for oxidative events in the IC1270-induced resistance mechanism.ConclusionBesides identifying ROS as modulators of antagonistic defense mechanisms in rice, this work reveals the mechanistic similarities between S. plymuthica-mediated ISR and R protein-dictated ETI and underscores the importance of using appropriate innate defense mechanisms when breeding for broad-spectrum rice disease resistance.
Highlights
Induced resistance is a state of enhanced defensive capacity developed by a plant reacting to specific biotic or chemical stimuli
Cultivation of rhizobacteria and pathogens Bacterial strains used in this study were Serratia plymuthica IC1270, which was originally described as Enterobacter agglomerans [29], and Pseudomonas aeruginosa 7NSK2 [33]
Differential effectiveness of induced systemic resistance (ISR) triggered by S. plymuthica IC1270 To assess the ISR-triggering capacity of S. plymuthica IC1270, susceptible rice plants were grown in soil containing IC1270 bacteria, and subsequently challenged with several fungal pathogens exhibiting different modes of infection
Summary
Induced resistance is a state of enhanced defensive capacity developed by a plant reacting to specific biotic or chemical stimuli. PTI is triggered by recognition of pathogen- or microbial-associated molecular patterns (PAMPs/ MAMPs), which are conserved molecular signatures decorating many classes of microbes, including non-pathogens. Perception of MAMPs by pattern recognition receptors (PRRs) at the cell surface activates a battery of host defense responses leading to a basal level of resistance [3]. As a result of the evolutionary arms-race between plants and their intruders, many microbial pathogens acquired the ability to dodge PTI-based host surveillance via secretion of effector molecules that intercept MAMPtriggered defense signals [4]. Plants have adapted to produce cognate R-(resistance) proteins by which they recognize, either directly or indirectly, these pathogenspecific effector proteins, resulting in a superimposed layer of defense variably termed effector-triggered immunity (ETI), gene-for-gene resistance or R-gene-dependent resistance [1]
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