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Research in the past decade suggests that the outcome of an interaction between a plant and a pathogen depends on a series of complex signaling pathways (Kunkel & Brooks, 2002). However, much of the research has been focused on the activation of defense signaling pathways by the interaction between resistance (R) genes in the host and the corresponding avirulence (avr) genes in the pathogen, also known as ‘gene-for-gene’ (GFG) resistance (reviewed by Dangl & Jones, 2001; Dangl & McDowell, 2006). While GFG resistance seems to be prevalent among plant–pathogen interactions (Hammond-Kosack & Jones, 1997), other mechanisms also contribute to plant defense (Glazebrook et al., 1996; Sticher et al., 1997; Dewdney et al., 2000; Jones & Takemoto, 2004; Diener & Ausubel, 2005). In particular, it has been shown that variation in resistance among crops and natural populations is often quantitative (Young, 1996; Kover & Caicedo, 2001; Denby et al., 2004). The fact that most natural interactions vary quantitatively, together with numerous examples of single-gene resistance being quickly overcome in crops (Strange & Scott, 2005), has led to the suggestion that quantitative resistance is more durable than qualitative resistance. Yet, the molecular basis of quantitative variation in disease resistance remains mostly unknown.
Pathogens represent one of the biggest challenges in increasing plant yield, because of their large effects on crop growth, productivity and quality (Strange & Scott, 2005). Characterization of the genetic basis of disease resistance offers a promising avenue for the development of new resistant varieties by transferring resistance genes into crops (Stuiver & Custers, 2001) or by performing marker-assisted selection (Strange & Scott, 2005). However, these avenues will only be successful if resistance genes directly cause an increase in fitness and are not costly, assumptions that are not usually tested in the model organisms used to identify resistance genes.
The interaction between Arabidopsis thaliana and Pseudomonas syringae has been one of the primary pathosystems in which the molecular basis of plant resistance has been studied (reviewed in Dangl & Jones, 2001; Katagiri et al., 2002; Thatcher et al., 2005). Pseudomonas syringae is a bacterial plant pathogen known to cause disease on a variety of important crop plants (Hirano & Upper, 2000), and it has also been observed in natural populations of A. thaliana (Jakob et al., 2002). The possibility of transforming the strain Pst DC3000 (isolated originally from tomato (Lycopersicon esculentum)) with single avr genes has allowed the identification of five R genes and a number of other genes involved in the resistance pathway (Katagiri et al., 2002; Meyers et al., 2003). Recently, a survey of 19 natural accessions of A. thaliana has shown the existence of quantitative variation in susceptibility to Pst DC3000 (Kover & Schaal, 2002). This finding provided the opportunity to investigate the molecular basis of quantitative variation in susceptibility and its possible relationship to qualitative variation.
Quantitative variation in disease susceptibility is typically polygenic and affected by the environment (Young, 1996). Thus, to better understand the genetic basis of the quantitative variation in susceptibility to Pst DC3000 in A. thaliana, we performed two quantitative trait locus (QTL) studies. The first study investigated the genetic basis of quantitative variation in susceptibility among the F2 progeny of accessions Nossen (No-0) and Columbia (Col-0) (Kover et al., 2005), and found a few QTLs of small effect on symptom severity score. Here, we report the results of the second QTL analysis, which was performed on the F2 progeny of a cross between accessions Col-0 and San Feliu-2 (Sf-2). These two accessions represent the extremes of the quantitative variation in disease susceptibility previously observed (Kover & Schaal, 2002), and are consequently more variable than No-0 and Col-0. In addition, Sf-2 has been previously reported to be resistant to a number of P. syringae strains, including Pst DC3000 (Whalen et al., 1991).
In this study we investigate the genetic basis of the difference in susceptibility between Sf-2 and Col-0, the possible interaction between QTLs for susceptibility and environmental conditions, and the effect of QTLs for susceptibility on fruit production (plant yield). In contrast to the first QTL study, we found that differences between accessions Col-0 and Sf-2 in susceptibility to Pst DC3000 can be largely explained by a single genetic factor mapping to the bottom of chromosome 5. This previously unknown genetic factor, which behaves in the manner typical of classical plant R genes, equally affects bacterial growth and disease symptom development, but has no effect on fruit production. Although this QTL explained most of the variation, two other QTLs of small and environmentally dependent effect were also detected on chromosomes 1 and 4. Although QTLs for fruit production were observed, QTLs for susceptibility did not have any effect on fruit production.