A role for tocopherol biosynthesis in Arabidopsis thaliana basal immunity to bacterial infection.
Mo kle
Abstrè
Tocopherols are lipid-soluble antioxidants synthesized in plastids of higher plants and other photosynthetic organisms. The four known tocopherols alpha-, beta-, gamma- and delta-tocopherol differ in number and position of methyl groups on their chromanol head group. In unstressed Arabidopsis thaliana leaves, alpha-tocopherol constitutes the main tocopherol form, whereas seeds predominantly contain gamma-tocopherol. Here, we show that inoculation of Arabidopsis leaves with the bacterial pathogen Pseudomonas syringae induces expression of genes involved in early steps of tocopherol biosynthesis, and triggers strong accumulation of gamma-tocopherol, moderate production of delta-tocopherol, and generation of the benzoquinol precursors of tocopherols. The pathogen-inducible biosynthesis of tocopherols is promoted by the immune regulators ENHANCED DISEASE SUSCEPTIBILITY1 and PHYTOALEXIN-DEFICIENT4. In addition, tocopherols accumulate in response to bacterial flagellin and reactive oxygen species. By assessing the content and composition of tocopherol forms in naïve and inoculated plants of wild-type and tocopherol biosynthetic pathway mutants, we provide biochemical insights into the pathogen-inducible tocopherol pathway. Notably, vte2 mutant plants, which are compromised in both tocopherol and benzoquinol precursor accumulation, exhibit increased susceptibility towards compatible P. syringae and possess heightened levels of markers of lipid peroxidation after bacterial infection. The deficiency of tri-unsaturated fatty acids in vte2-1 fad3-2 fad7-2 fad8 quadruple mutants prevents increased lipid peroxidation in the vte2 background and restores pathogen resistance to wild-type levels. Therefore, the tocopherol biosynthetic pathway positively influences SA biosynthesis and guarantees effective basal resistance of Arabidopsis against compatible P. syringae bacteria, possibly by protecting leaves from the pathogen-induced oxidation of trienoic fatty acid-containing lipids.