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Analysis of new type III effectors from Xanthomonas uncovers XopB and XopS as suppressors of plant immunity
Author(s) -
Schulze Sebastian,
Kay Sabine,
Büttner Daniela,
Egler Monique,
EschenLippold Lennart,
Hause Gerd,
Krüger Antje,
Lee Justin,
Müller Oliver,
Scheel Dierk,
Szczesny Robert,
Thieme Frank,
Bonas Ulla
Publication year - 2012
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/j.1469-8137.2012.04210.x
Subject(s) - effector , biology , xanthomonas campestris , xanthomonas , plant immunity , vacuole , secretion , type three secretion system , microbiology and biotechnology , pathogen , plant defense against herbivory , mutant , immunity , protoplast , cytoplasm , gene , genetics , arabidopsis , immune system , biochemistry
Summary• The pathogenicity of the Gram‐negative plant‐pathogenic bacterium Xanthomonas campestris pv. vesicatoria ( Xcv ) is dependent on type III effectors (T3Es) that are injected into plant cells by a type III secretion system and interfere with cellular processes to the benefit of the pathogen. • In this study, we analyzed eight T3Es from Xcv strain 85‐10, six of which were newly identified effectors. Genetic studies and protoplast expression assays revealed that XopB and XopS contribute to disease symptoms and bacterial growth, and suppress pathogen‐associated molecular pattern (PAMP)‐triggered plant defense gene expression. • In addition, XopB inhibits cell death reactions induced by different T3Es, thus suppressing defense responses related to both PAMP‐triggered immunity (PTI) and effector‐triggered immunity (ETI). • XopB localizes to the Golgi apparatus and cytoplasm of the plant cell and interferes with eukaryotic vesicle trafficking. Interestingly, a XopB point mutant derivative was defective in the suppression of ETI‐related responses, but still interfered with vesicle trafficking and was only slightly affected with regard to the suppression of defense gene induction. This suggests that XopB‐mediated suppression of PTI and ETI is dependent on different mechanisms that can be functionally separated.