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Wide quantitative variation in plant disease resistance across Arabidopsis wild populations has been documented and the underlying mechanisms remain largely unknown. To investigate the genetic and molecular basis of this variation, Arabidopsis recombinant inbred lines (RILs) derived from Aa-0 × Col-0 and Gie-0 × Col-0 crosses were constructed and used for inoculation with  Pseudomonas syringae  pathovars  maculicola  ES4326 (ES4326) and  tomato  DC3000 (DC3000). Bacterial growth assays revealed continuous distribution across the large differences between the most and the least susceptible lines in the RILs. Quantitative trait locus (QTL) mapping analyses identified a number of QTLs underpinning the variance in disease resistance, among which  Qpm3.1 , a major QTL on chromosome III from both Aa-0 and Gie-0 accessions, preferentially restricted the growth of ES4326. A genetic screen for the ES4326 gene selectively leading to bacterial growth inhibition on accession Aa-0 uncovered the effector gene  hopW1-1 . Further QTL analysis of disease in RILs inoculated with DC3000 carrying  hopW1-1  showed that the genetic interaction between  Qpm3.1  and  hopW1-1  determined Arabidopsis resistance to bacterial infection. These findings illustrate the complexity of Arabidopsis- Pseudomonas  interaction and highlight the importance of pathogen effectors in delineating genetic architectures of quantitative variation in plant disease resistance.

frontiers in plant science

Genetic Interaction between Arabidopsis Qpm3.1 Locus and Bacterial Effector Gene hopW1-1 Underlies Natural Variation in Quantitative Disease Resistance to Pseudomonas Infection