Abstract
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.
Highlights
Citrus canker, caused by Xanthomonas citri pv. citri (Xcc), is one of the most devastating diseases affecting citrus production worldwide [1]
To better understand the molecular mechanisms underlying disease development, we previously focused on the identification and characterization of several bacterial components involved in Xcc virulence such as type III and type V protein secretion systems [2,3], the exopolysaccharide xanthan [4] and a Xcc plant natriuretic peptide-like protein (XacPNP) [5]
We observed that the expression of XacPNP is induced upon infection and that lesions produced in leaves infected with a XacPNP deletion mutant were more necrotic than those observed with the wild type and the highly necrotic tissue led to earlier bacterial cell death in the mutant
Summary
Citrus canker, caused by Xanthomonas citri pv. citri (Xcc), is one of the most devastating diseases affecting citrus production worldwide [1]. To better understand the molecular mechanisms underlying disease development, we previously focused on the identification and characterization of several bacterial components involved in Xcc virulence such as type III and type V protein secretion systems [2,3], the exopolysaccharide xanthan [4] and a Xcc plant natriuretic peptide-like protein (XacPNP) [5]. We observed that the expression of XacPNP is induced upon infection and that lesions produced in leaves infected with a XacPNP deletion mutant were more necrotic than those observed with the wild type and the highly necrotic tissue led to earlier bacterial cell death in the mutant This suggests that the plant-like bacterial PNP enables the plant pathogen to modify host responses in order to create conditions favorable to its own survival [5,7]. We discuss the effect of XacPNP on the primary metabolism of the host plant and the consequences on the arms race between the pathogen and the host
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