Eukaryotic-Acquired Gene by a Biotrophic Phytopathogen Allows Prolonged Survival on the Host by Counteracting the Shut-Down of Plant Photosynthesis

Xanthomonas citri pv. citri, the bacteria responsible for citrus canker posses a biological active plant natriuretic peptide (PNP)-like protein, not present in any other bacteria. PNPs are a class of extracellular, systemically mobile peptides that elicit a number of plant responses important in hom...

Full description

Saved in:
Bibliographic Details
Published inPloS one Vol. 5; no. 1; p. e8950
Main Authors Garavaglia, Betiana S, Thomas, Ludivine, Gottig, Natalia, Dunger, Germán, Garofalo, Cecilia G, Daurelio, Lucas D, Ndimba, Bongani, Orellano, Elena G, Gehring, Chris, Ottado, Jorgelina
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 28.01.2010
Public Library of Science (PLoS)
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Xanthomonas citri pv. citri, the bacteria responsible for citrus canker posses a biological active plant natriuretic peptide (PNP)-like protein, not present in any other bacteria. PNPs are a class of extracellular, systemically mobile peptides that elicit a number of plant responses important in homeostasis and growth. Previously, we showed that a Xanthomonas citri pv. citri mutant lacking the PNP-like protein XacPNP produced more necrotic lesions in citrus leaves than wild type infections and suggested a role for XacPNP in the regulation of host homeostasis. Here we have analyzed the proteome modifications observed in citrus leaves infected with the wild type and XacPNP deletion mutant bacteria. While both of them cause down-regulation of enzymes related to photosynthesis as well as chloroplastic ribosomal proteins, proteins related to defense responses are up-regulated. However, leaves infiltrated with the XacPNP deletion mutant show a more pronounced decrease in photosynthetic proteins while no reduction in defense related proteins as compared to the wild-type pathogen. This suggests that XacPNP serves the pathogen to maintain host photosynthetic efficiency during pathogenesis. The results from the proteomics analyses are consistent with our chlorophyll fluorescence data and transcript analyses of defense genes that show a more marked reduction in photosynthesis in the mutant but no difference in the induction of genes diagnostic for biotic-stress responses. We therefore conclude that XacPNP counteracts the shut-down of host photosynthesis during infection and in that way maintains the tissue in better conditions, suggesting that the pathogen has adapted a host gene to modify its natural host and render it a better reservoir for prolonged bacterial survival and thus for further colonization.
Bibliography:http://dx.doi.org/10.1371/journal.pone.0008950
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Conceived and designed the experiments: BSG LT NG GD CGG LDD BN EGO CG JO. Performed the experiments: BSG LT GD CGG LDD. Analyzed the data: BSG LT NG GD CGG BN EGO CG JO. Contributed reagents/materials/analysis tools: NG BN EGO CG JO. Wrote the paper: BSG LT NG GD BN CG JO.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0008950