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The P seudomonas type III effector HopQ1 activates cytokinin signaling and interferes with plant innate immunity
Author(s) -
Hann Dagmar R.,
DomínguezFerreras Ana,
Motyka Vaclav,
Dobrev Petre I.,
Schornack Sebastian,
Jehle Anna,
Felix Georg,
Chinchilla Delphine,
Rathjen John P.,
Boller Thomas
Publication year - 2014
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.12544
Subject(s) - cytokinin , flagellin , biology , effector , signal transduction , microbiology and biotechnology , mutant , innate immune system , biochemistry , receptor , gene , auxin
Summary We characterized the molecular function of the P seudomonas syringae pv. tomato DC 3000 ( Pto ) effector HopQ1. In silico studies suggest that HopQ1 might possess nucleoside hydrolase activity based on the presence of a characteristic aspartate motif. Transgenic A rabidopsis lines expressing HopQ1 or HopQ1 aspartate mutant variants were characterized with respect to flagellin triggered immunity, phenotype and changes in phytohormone content by high‐performance liquid chromatography‐MS ( HPLC ‐ MS ). We found that HopQ1, but not its aspartate mutants, suppressed all tested immunity marker assays. Suppression of immunity was the result of a lack of the flagellin receptor FLS 2, whose gene expression was abolished by HopQ1 in a promoter‐dependent manner. Furthermore, HopQ1 induced cytokinin signaling in A rabidopsis and the elevation in cytokinin signaling appears to be responsible for the attenuation of FLS2 expression. We conclude that HopQ1 can activate cytokinin signaling and that moderate activation of cytokinin signaling leads to suppression of FLS2 accumulation and thus defense signaling.