Genetic variation for induced and basal resistance against leaf pathogen Pseudomonas syringae pv. tomato DC3000 among Arabidopsis thaliana accessions
Genetic variation for induced and basal resistance against leaf pathogen Pseudomonas syringae pv. tomato DC3000 among Arabidopsis thaliana accessions
In Arabidopsis thaliana, significant efforts to determine the effect of naturally occurring variation between phenotypically divergent accessions on different biotic or abiotic stresses are underway. Although it is usually assumed that induced systemic resistance (ISR) against pathogen will covary with plant genetic variation, this assumption has not been tested rigorously in previous experiments. Here, we investigated heritable variation in resistance as well as Penicillium simplicissimum GP17-2-mediated ISR to the bacteria Pseudomonas syringae pv. tomato DC3000 (Pst) among a worldwide collection of accessions of A. thaliana. In this study, 75 Arabidopsis accessions were screened against the bacteria Pst following induction and non-induction treatment and their resistance levels were determined by measuring three components of A. thaliana resistance (infected leaf number, disease severity and pathogen growth). We observed extensive quantitative variation in the number of infected leaves, severity of disease symptoms and the bacterial population size among 75 accessions of A. thaliana infected with Pst. On the contrary, about a two-third of the accessions (49 accessions) showed a reduction in infected leaf number, disease severity and pathogen proliferation after treatment with GP17-2, indicating that GP17-2 induction of resistance is ecotype specific in Arabidopsis. The level of suppression was more pronounced for percent disease severity and pathogen proliferation than for number of infected leaves in ISR-inducible accessions. Accessions non-responsive to GP17-2 treatment generally appeared to be associated with higher basal resistance to infection by Pst. Future study with these parental lines employing a variety of crossing schemes may facilitate identification of major trait loci responsible for GP17-2-mediated ISR in Arabidopsis.
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