Liesl Van der Linden,1
Katherine J. Denby,3
Yves Marco,4 and
Dave K. Berger1
1Department of Plant Science and 2Department of Genetics, Forestry and Agricultural Research Institute (FABI), University of Pretoria, 0028, South Africa; 3School of Life Sciences and Warwick Systems Biology Centre, University of Warwick, U.K.; 4Laboratoire des Interactions Plantes-Microorganismes, UMR CNRS/INRA 2594/441, 31320 Castanet-Tolosan, France
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Accepted 5 December 2012.
Bacterial wilt caused by Ralstonia solanacearum is a disease of widespread economic importance that affects numerous plant species, including Arabidopsis thaliana. We describe a pathosystem between A. thaliana and biovar 3 phylotype I strain BCCF402 of R. solanacearum isolated from Eucalyptus trees. A. thaliana accession Be-0 was susceptible and accession Kil-0 was tolerant. Kil-0 exhibited no wilting symptoms and no significant reduction in fitness (biomass, seed yield, and germination efficiency) after inoculation with R. solanacearum BCCF402, despite high bacterial numbers in planta. This was in contrast to the well-characterized resistance response in the accession Nd-1, which limits bacterial multiplication at early stages of infection and does not wilt. R. solanacearum BCCF402 was highly virulent because the susceptible accession Be-0 was completely wilted after inoculation. Genetic analyses, allelism studies with Nd-1, and RRS1 cleaved amplified polymorphic sequence marker analysis showed that the tolerance phenotype in Kil-0 was dependent upon the resistance gene RRS1. Knockout and complementation studies of the R. solanacearum BCCF402 effector PopP2 confirmed that the tolerance response in Kil-0 was dependent upon the RRS1–PopP2 interaction. Our data indicate that the gene-for-gene interaction between RRS1 and PopP2 can contribute to tolerance, as well as resistance, which makes it a useful model system for evolutionary studies of the arms race between plants and bacterial pathogens. In addition, the results alert biotechnologists to the risk that deployment of RRS1 in transgenic crops may result in persistence of the pathogen in the field.
© 2013 The American Phytopathological Society