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. 2010 May;185(1):283-91.
doi: 10.1534/genetics.109.112383. Epub 2010 Feb 8.

Impact of initial pathogen density on resistance and tolerance in a polymorphic disease resistance gene system in Arabidopsis thaliana

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Impact of initial pathogen density on resistance and tolerance in a polymorphic disease resistance gene system in Arabidopsis thaliana

Fabrice Roux et al. Genetics. 2010 May.

Abstract

The evolution of natural enemy defense shapes evolutionary trajectories of natural populations. Although the intensity of selection imposed by enemies clearly varies among natural populations, little is known about the reaction norm of genotypes under a gradient of selective pressure. In this study, we measure the quantitative responses of disease symptoms and plant fitness to a gradient of infection, focusing on the gene-for-gene interaction between the Rpm1 resistance gene in Arabidopsis thaliana and the AvrRpm1 avirulence gene in the bacterial pathogen Pseudomonas syringae. Two complementary sets of plant material were used: resistant (R) and susceptible (S) isogenic lines and a set of six natural accessions, three of which are Rpm1 resistant (R) and three of which are rpm1 susceptible (S). Nine initial pathogen densities were applied to each plant line. Using isogenic lines allows any differences between R and S lines to be attributed directly to the Rpm1 gene, whereas using natural accessions allows the natural variation of resistance and tolerance over a gradient of infection dosages within R and S accessions to be described. For both sets of plant material, increased infection dosage results in more extensive disease symptoms, with a subsequent decrease in seed production. The severity of disease symptoms was reduced in R relative to S subgroups, and the presence of the Rpm1 allele led to an increase in plant fitness. Tolerance, defined as the ability to sustain infection without a reduction in fitness, was directly affected by Rpm1, providing a novel demonstration of an R gene affecting tolerance. Genetic variation for tolerance was also found within the S and R natural accessions, suggesting the potential for selection to act upon this important trait.

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Figures

F<sc>igure</sc> 1.—
Figure 1.—
Effect of Rpm1 resistance on disease symptoms 5 days after infection (Symp5D) under nine different initial inoculation densities. (A) Isogenic lines; (B) natural accessions. Mean and SEM for Symp5D were plotted by initial inoculation densities. Planned comparisons were made for R vs. S for each infection dosage: (*) 0.05 > P > 0.01. (**) 0.01 > P > 0.001. (***) P < 0.001. No asterisk means not significant.
F<sc>igure</sc> 2.—
Figure 2.—
Effect of Rpm1 resistance on plant fitness, measured as total silique length (TSL), under nine different initial inoculation densities. (A) Isogenic lines; (B) natural accessions. Mean and SEM for TSL were plotted by initial inoculation densities. Planned comparisons were made for R vs. S for each infection dosage: (*) 0.05 > P > 0.01. (**) 0.01 > P > 0.001. (***) P < 0.001. No asterisk means not significant.
F<sc>igure</sc> 3.—
Figure 3.—
Effect of disease symptoms 5 days after infection (Symp5D) on plant fitness, measured as total silique length (TSL). (A) Isogenic lines; (B) natural accessions. Mean and SEM for TSL were plotted by symptom levels.
F<sc>igure</sc> 4.—
Figure 4.—
Natural variation in tolerance among accessions within the S subgroup. Tolerance was measured as the relationship between fitness, measured as TSL, and disease symptoms 5 days after infection (Symp5D). Mean and SEM for TSL were plotted by symptom levels for Cvi-0 and Ga-0.

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