Sphingolipids are emerging as second messengers in programmed cell death and plant defense mechanisms. However, their role in plant defense is far from being understood, especially against necrotrophic pathogens. Sphingolipidomics and plant defense responses during pathogenic
infection were evaluated in the mutant of long-chain base
phosphate (LCB-P)
lyase, encoded by the
dihydrosphingosine-1-phosphate lyase1 (AtDPL1) gene and regulating long-chain base/LCB-P homeostasis. Atdpl1 mutants exhibit tolerance to the necrotrophic fungus Botrytis cinerea but susceptibility to the hemibiotrophic bacterium Pseudomonas syringae pv tomato (Pst). Here, a direct comparison of
sphingolipid profiles in Arabidopsis (Arabidopsis thaliana) during
infection with pathogens differing in lifestyles is described. In contrast to long-chain bases (
dihydrosphingosine [d18:0] and 4,8-
sphingadienine [d18:2]), hydroxyceramide and LCB-P (
phytosphingosine-1-
phosphate [t18:0-P] and 4-hydroxy-8-sphingenine-1-
phosphate [t18:1-P]) levels are higher in Atdpl1-1 than in wild-type plants in response to B. cinerea. Following Pst
infection, t18:0-P accumulates more strongly in Atdpl1-1 than in wild-type plants. Moreover, d18:0 and t18:0-P appear as key players in Pst- and B. cinerea-induced cell death and
reactive oxygen species accumulation.
Salicylic acid levels are similar in both types of plants, independent of the pathogen. In addition,
salicylic acid-dependent gene expression is similar in both types of B. cinerea-infected plants but is repressed in Atdpl1-1
after treatment with Pst.
Infection with both pathogens triggers higher
jasmonic acid,
jasmonoyl-isoleucine accumulation, and
jasmonic acid-dependent gene expression in Atdpl1-1 mutants. Our results demonstrate that
sphingolipids play an important role in plant defense, especially toward necrotrophic pathogens, and highlight a novel connection between the
jasmonate signaling pathway, cell death, and
sphingolipids.