Pseudomonas syringae infection triggers de novo synthesis of phytosphingosine from sphinganine in Arabidopsis thaliana

Sphingolipids are important membrane components and also regulate cell proliferation and apoptosis. We detected a fast increase of the free sphingobase t18:0 (phytosphinganine) in Arabidopsis leaves after inoculation with an avirulent strain of the bacterial pathogen Pseudomonas syringae pathovar tomato , characterized by host cell death reactions. The induction of phytosphinganine was more transient in virulent interactions lacking cell death reactions, suggesting a positive role of t18:0 in the plants’ response to pathogens, e.g. the hypersensitive response. In the mutant sphingobase hydroxylase 1 ( sbh1‐1 ), Pseudomonas induced elevated free d18:0 levels. As total t18:0 contents (after hydrolysis of ceramides) were not reduced in sbh1‐1 , the pathogen‐triggered t18:0 increase most likely results from de novo synthesis from d18:0 which would require SBH1.