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Naji, M. |
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Motta, Antonella |
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Aletan, Dirar |
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Mohamed, Tarek |
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Ertürk, Emre |
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Taccardi, Nicola |
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Kononenko, Denys |
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Petrov, R. H. | Madrid |
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Alshaaer, Mazen | Brussels |
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Bih, L. |
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Casati, R. |
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Muller, Hermance |
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Kočí, Jan | Prague |
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Šuljagić, Marija |
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Kalteremidou, Kalliopi-Artemi | Brussels |
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Azam, Siraj |
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Ospanova, Alyiya |
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Blanpain, Bart |
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Ali, M. A. |
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Popa, V. |
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Rančić, M. |
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Ollier, Nadège |
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Azevedo, Nuno Monteiro |
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Landes, Michael |
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Rignanese, Gian-Marco |
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Lisón, P.
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article
SlS5H silencing reveals specific pathogen-triggered salicylic acid metabolism in tomato
Abstract
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Salicylic acid (SA) is a major plant hormone that mediates the defence pathway against pathogens. SA accumulates in highly variable amounts depending on the plant-pathogen system, and several enzyme activities participate in the restoration of its levels. Gentisic acid (GA) is the product of the 5-hydroxylation of SA, which is catalysed by S5H, an enzyme activity regarded as a major player in SA homeostasis. GA accumulates at high levels in tomato plants infected by Citrus Exocortis Viroid (CEVd), and to a lesser extend upon <jats:italic>Pseudomonas syringae</jats:italic> DC3000 pv. <jats:italic>tomato</jats:italic> (<jats:italic>Pst</jats:italic>) infection.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We have studied the induction of tomato <jats:italic>SlS5H</jats:italic> gene by different pathogens, and its expression correlates with the accumulation of GA. Transient over-expression of <jats:italic>SlS5H</jats:italic> in <jats:italic>Nicotiana benthamiana</jats:italic> confirmed that SA is processed by SlS5H in vivo. <jats:italic>SlS5H</jats:italic>-silenced tomato plants were generated, displaying a smaller size and early senescence, together with hypersusceptibility to the necrotrophic fungus <jats:italic>Botrytis cinerea</jats:italic>. In contrast, these transgenic lines exhibited an increased defence response and resistance to both CEVd and <jats:italic>Pst</jats:italic> infections. Alternative SA processing appears to occur for each specific pathogenic interaction to cope with SA levels. In <jats:italic>SlS5H</jats:italic>-silenced plants infected with CEVd, glycosylated SA was the most discriminant metabolite found. Instead, in <jats:italic>Pst</jats:italic>-infected transgenic plants, SA appeared to be rerouted to other phenolics such as feruloyldopamine, feruloylquinic acid, feruloylgalactarate and 2-hydroxyglutarate.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Using <jats:italic>SlS5H</jats:italic>-silenced plants as a tool to unbalance SA levels, we have studied the re-routing of SA upon CEVd and <jats:italic>Pst</jats:italic> infections and found that, despite the common origin and role for SA in plant pathogenesis, there appear to be different pathogen-specific, alternate homeostasis pathways.</jats:p></jats:sec>