The combined action of 9 lipoxygenase and galactolipase is sufficient to bring about programmed cell death during tobacco hypersensitive response

Oxylipins, derived from fatty acid hydroperoxides (FAHs), are thought to play different roles during plant pathogen interactions. During hypersensitive response (HR) some of them serve as signals necessary for defence gene activation whereas others could contribute to pathogen killing or could participate in the execution of plant programmed cell death (PCD) associated with this resistance. In order to address the role of these compounds in the latter process, we have closely observed lipid peroxidation, the first step of this metabolic pathway, under different situations which led either to accelerated or inhibited HR cell death. The oxidative process has been studied in cryptogein-elicited tobacco leaves and during Ralstonia solanacearum-induced HR. It was shown that FAH accumulation was preceded by the co-ordinated rise in 9 lipoxygenase (9 LOX) and galactolipase activities in addition to the transcription of a set of four genes encoding 9 LOX and patatin-like proteins, NtPAT1-3. The latter gene expression was at the origin of a metabolic pathway allowing the release of poly-unsaturated fatty acids from plastid galactolipids and their oxidation into free 9 FAHs. This 9 LOX-dependent lipid peroxidation was found to be sufficient to lead to HR cell death. Finally, during the bacterial-induced HR, lipid peroxidation appeared as a composite of metabolites of enzymatic and non-enzymatic origins and suggested the role of H2O2 as an important source of oxidant that might, in synergy with 9 FAHs, contribute to cell death execution.