| Summary: | <p>Abstract</p> <p>Background</p> <p>Grapevine protection against diseases needs alternative strategies to the use of phytochemicals, implying a thorough knowledge of innate defense mechanisms. However, signalling pathways and regulatory elements leading to induction of defense responses have yet to be characterized in this species. In order to study defense response signalling to pathogens in <it>Vitis vinifera</it>, we took advantage of its recently completed genome sequence to characterize two putative orthologs of <it>NPR1</it>, a key player in salicylic acid (SA)-mediated resistance to biotrophic pathogens in <it>Arabidopsis thaliana</it>.</p> <p>Results</p> <p>Two cDNAs named <it>VvNPR1.1 </it>and <it>VvNPR1.2 </it>were isolated from <it>Vitis vinifera </it>cv Chardonnay, encoding proteins showing 55% and 40% identity to Arabidopsis NPR1 respectively. Constitutive expression of <it>VvNPR1.1 </it>and <it>VvNPR1.2 </it>monitored in leaves of <it>V. vinifera </it>cv Chardonnay was found to be enhanced by treatment with benzothiadiazole, a SA analog. In contrast, <it>VvNPR1.1 </it>and <it>VvNPR1.2 </it>transcript levels were not affected during infection of resistant <it>Vitis riparia </it>or susceptible <it>V. vinifera </it>with <it>Plasmopara viticola</it>, the causal agent of downy mildew, suggesting regulation of VvNPR1 activity at the protein level. VvNPR1.1-GFP and VvNPR1.2-GFP fusion proteins were transiently expressed by agroinfiltration in <it>Nicotiana benthamiana </it>leaves, where they localized predominantly to the nucleus. In this system, <it>VvNPR1.1 </it>and <it>VvNPR1.2 </it>expression was sufficient to trigger the accumulation of acidic SA-dependent Pathogenesis-Related proteins PR1 and PR2, but not of basic chitinases (PR3) in the absence of pathogen infection. Interestingly, when <it>VvNPR1.1 </it>or <it>AtNPR1 </it>were transiently overexpressed in <it>Vitis vinifera </it>leaves, the induction of grapevine <it>PR1 </it>was significantly enhanced in response to <it>P. viticola</it>.</p> <p>Conclusion</p> <p>In conclusion, our data identified grapevine homologs of NPR1, and their functional analysis showed that VvNPR1.1 and VvNPR1.2 likely control the expression of SA-dependent defense genes. Overexpression of <it>VvNPR1 </it>has thus the potential to enhance grapevine defensive capabilities upon fungal infection. As a consequence, manipulating <it>VvNPR1 </it>and other signalling elements could open ways to strengthen disease resistance mechanisms in this crop species.</p>
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