Resistance to phytopathogens e tutti quanti : placing plant quantitative disease resistance on the map

Plant disease resistance can be seen as a process of a dual nature: both qualitative and quantitative.The nature of non-self molecules perceived by plants has led to the depiction of plant immunity as a two-layer defence system. The first layer is mediated by cell surface and intracellular pattern recognition receptors (PRRs) which perceive conserved microbial elicitors, termed pathogenassociated molecular patterns (PAMPs). The perception of these conserved elicitors initiates cascades of signalling and transcription events, known as PAMP-triggered immunity (PTI). Adapted pathogens secrete effector molecules able to suppress PTI, but which may also be recognized by plant intracellular resistance (R) proteins. This initiates effector-triggered immunity (ETI), the second layer of plant defence. ETI typically yields complete disease resistance phenotypes against pathogens containing the recognized effector, a process designated as qualitative resistance. By contrast, perception of a single PAMP typically has a weaker contribution to overall plant resistance. More generally, in the absence of qualitative resistance, an incomplete resistance phenomenon is often observed, leading to a reduction rather than absence of disease. This is usually referred to as quantitative disease resistance (QDR). The definition of QDR varies in the literature according to the interests of the authors, so that the QDR concept may be puzzling. We settled to define QDR based on the simultaneous occurrence of two observations: (i) the disease resistance phenotype follows a continuous distribution from susceptibility to resistance in host populations, as opposed to the ‘susceptibility or resistance’ binary phenotype observed in qualitative resistance (Fig. 1A); and (ii) the disease resistance phenotype is determined by multiple quantitative trait loci (QTLs) as revealed by crossing host parents with contrasted phenotypes. As a consequence, full disease resistance can be achieved by the introduction of a single R gene, but not by the introduction of a single QDR gene, in a susceptible genetic background. Based on this definition, the molecular architecture of QDR can be hypothesized as an intricate network integrating multiple response pathways to several pathogen molecular determinants and environmental cues (Fig. 1B). THE QUALITATIVE–QUANTITATIVE DUALITY OF PLANT DISEASE RESISTANCE