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Xanthomonas axonopodis pv. citri uses a plant natriuretic peptide-like protein to modify host homeostasis
Author(s) -
Natalia Gottig,
Betiana S. Garavaglia,
Lucas D. Daurelio,
Alex J. Valentine,
Chris Gehring,
Elena G. Orellano,
Jorgelina Ottado
Publication year - 2008
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.0810107105
Subject(s) - biology , xanthomonas , pseudomonas syringae , mutant , microbiology and biotechnology , pathogen , bacteria , apoplast , arabidopsis , host (biology) , npr1 , gene , botany , genetics , cell wall , natriuretic peptide , medicine , heart failure
Plant natriuretic peptides (PNPs) are a class of extracellular, systemically mobile molecules that elicit a number of plant responses important in homeostasis and growth. The bacterial citrus pathogen,Xanthomonas axonopodis pv.citri , also contains a gene encoding a PNP-like protein, XacPNP, that shares significant sequence similarity and identical domain organization with plant PNPs but has no homologues in other bacteria. We have expressed and purified XacPNP and demonstrated that the bacterial protein alters physiological responses including stomatal opening in plants. AlthoughXacPNP is not expressed under standard nutrient rich culture conditions, it is strongly induced under conditions that mimic the nutrient poor intercellular apoplastic environment of leaves, as well as in infected tissue, suggesting thatXacPNP transcription can respond to the host environment. To characterize the role of XacPNP during bacterial infection, we constructed aXacPNP deletion mutant. The lesions caused by this mutant were more necrotic than those observed with the wild-type, and bacterial cell death occurred earlier in the mutant. Moreover, when we expressedXacPNP inXanthomonas axonopodis pv.vesicatoria , the transgenic bacteria caused less necrotic lesions in the host than the wild-type. In conclusion, we present evidence that a plant-like bacterial PNP can enable a plant pathogen to modify host responses to create conditions favorable to its own survival.

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