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Background  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  Vitis vinifera , we took advantage of its recently completed genome sequence to characterize two putative orthologs of  NPR1 , a key player in salicylic acid (SA)-mediated resistance to biotrophic pathogens in  Arabidopsis thaliana .    Results  Two cDNAs named  VvNPR1.1  and  VvNPR1.2  were isolated from  Vitis vinifera  cv Chardonnay, encoding proteins showing 55% and 40% identity to Arabidopsis NPR1 respectively. Constitutive expression of  VvNPR1.1  and  VvNPR1.2  monitored in leaves of  V. vinifera  cv Chardonnay was found to be enhanced by treatment with benzothiadiazole, a SA analog. In contrast,  VvNPR1.1  and  VvNPR1.2  transcript levels were not affected during infection of resistant  Vitis riparia  or susceptible  V. vinifera  with  Plasmopara viticola , 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  Nicotiana benthamiana  leaves, where they localized predominantly to the nucleus. In this system,  VvNPR1.1  and  VvNPR1.2  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  VvNPR1.1  or  AtNPR1  were transiently overexpressed in  Vitis vinifera  leaves, the induction of grapevine  PR1  was significantly enhanced in response to  P. viticola .    Conclusion  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  VvNPR1  has thus the potential to enhance grapevine defensive capabilities upon fungal infection. As a consequence, manipulating  VvNPR1  and other signalling elements could open ways to strengthen disease resistance mechanisms in this crop species.

Characterization of Vitis vinifera NPR1 homologs involved in the regulation of Pathogenesis-Related gene expression