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Pseudomonas syringae infection triggers de novo synthesis of phytosphingosine from sphinganine in Arabidopsis thaliana
Author(s) -
Peer Markus,
Stegmann Martin,
Mueller Martin J.,
Waller Frank
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.08.027
Subject(s) - pseudomonas syringae , virulence , biology , arabidopsis thaliana , microbiology and biotechnology , pathogen , mutant , programmed cell death , hypersensitive response , sphingosine , pseudomonadaceae , biochemistry , pseudomonas , apoptosis , bacteria , gene , genetics , receptor
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.