Abstract:
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.
