Abstract
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.
Highlights
Plants rely on a complex innate immune system to ward off pathogen attacks
Among Qpm loci, the prominent effect of Qpm3.1 was detected from both Col × Aa and Col × Gie recombinant inbred lines (RILs) challenged with ES4326 but was absent when inoculated with DC3000
This locus coincides with the major quantitative trait locus (QTL) QRps.JIC3.1 that has been identified during infection of Col × Ler RILs with the strain ES4326 (Rant et al, 2013), indicating that these two QTLs may be the same and potentially strain-specific and broadly exist in Arabidopsis accessions
Summary
Plants rely on a complex innate immune system to ward off pathogen attacks. Perception of pathogen-associated molecular patterns (PAMPs) by plant cell surface distributed receptors elicits the first line of defense-PAMP triggered immunity (PTI). A number of genes mediating quantitative disease resistance have been successfully cloned from major crop plants including wheat (Fu et al, 2009; Krattinger et al, 2009), rice (Fukuoka et al, 2009; Hayashi et al, 2010), maize (Hurni et al, 2015; Zuo et al, 2015) and soybean (Cook et al, 2012) Many of these genes provide durable resistance in the field and encode proteins distinct to typical R proteins, indicating that quantitative disease resistance and R-gene mediated resistance may recruit different components to deploy
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