CONICET | Buscador de Institutos y Recursos Humanos

Although plants accumulate high levels of L-proline (Pro) under stress conditions, their exposure to external Pro induce cell death. The activation of Pro-dehydrogenase (ProDH) occurring under this condition is suspected to be a cause for this detrimental effect. ProDH activation leads to accumulation of the toxic intermediate P5C, and may also enhance the reactive oxygen species (ROS) content by overload of the mitochondrial electron transport chain. Interestingly, we have recently found that Arabidopsis cells triggering the Hypersensitive Response (HR) induce the expression of ProDH genes (ProDH1 and ProDH2), and activate ProDH before cell death initiation. We have also observed that Arabidopsis ProDH silenced plants displayed reduced hypersensitive cell death. Considering that both Arabidopsis ProDH isoforms have non-redundant functions during abiotic stresses, we here analyzed if these isoforms differentially respond to biotic stresses. We evaluated the sensitivity of Arabidopsis ProDH1 and ProDH2 genes to exogenous salicylic acid (SA) and jasmonic acid (JA), the major hormones signalling pathogen defences. We also analyzed how these genes respond to avirulent pathogen in sid2 and npr1 mutant plants deficient in the SA-pathway. In both kinds of experiments ProDH1 and ProDH2 displayed differential activation. We next determined the susceptibility of two individual knockout ProDH mutant plants (prodh-1 and prodh-2) to virulent and avirulent isolates of Pseudomonas syringae pv. tomato. We observed similar susceptibility to the virulent pathogen in both mutants, but differences in their resistance to the avirulent bacteria. Reduction in HR cell death was similar in both knockouts plants. Altogether, these results support distinctive roles of both ProDH isoforms during biotic defence responses pointing out a role for Pro catabolism in plant immunity.

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