Incompatible plant-pathogen interactions trigger a known type of programmed cell death (PCD), the Hypersensitive Response (HR), at the infection sites. The biochemical signals promoting PCD in HR remains to be investigated. We recently described net alterations of the L-Proline (Pro) metabolism in HR. In addition, accumulation of Ä1-Pyrroline-5-carboxilate (P5C), an intermediate of Pro degradation, was proposed to induce PCD. Hence, we analyzed the putative effects of P5C along HR development. We used Arabidopsis thaliana cell suspension cultures infected with Pseudomonas syringae strains to produce or not HR (incompatible and compatible interactions, respectively). We evaluated by RT-PCR the transcriptional regulation of the genes implicated in Pro catabolism, Pro-dehydrogenase (ProDH) and P5C-dehydrogenase (P5CDH), along infection. Rapid induction of ProDH and a repression of P5CDH were only observed in incompatible interactions. The uncoupled expression of these genes is suspected to cause P5C accumulation. We found that these transcriptional changes parallel the second phase of the oxidative burst and the alkaline pH shift, and they precede cell death. Interestingly, pre-treatment of cells with a specific ProDH inhibitor abolishes pathogen-induced cell death. Taking together these results suggest that P5C is a key component of HR during plant-pathogen incompatible interactions.
