Abstract
Key messageResistance factors against non-adapted powdery mildews were mapped in barley. Some QTLs seem effective only to non-adapted mildews, while others also play a role in defense against the adapted form.The durability and effectiveness of nonhost resistance suggests promising practical applications for crop breeding, relying upon elucidation of key aspects of this type of resistance. We investigated which genetic factors determine the nonhost status of barley (Hordeum vulgare L.) to powdery mildews (Blumeria graminis). We set out to verify whether genes involved in nonhost resistance have a wide effectiveness spectrum, and whether nonhost resistance genes confer resistance to the barley adapted powdery mildew. Two barley lines, SusBgtSC and SusBgtDC, with some susceptibility to the wheat powdery mildew B. graminis f.sp. tritici (Bgt) were crossed with cv Vada to generate two mapping populations. Each population was assessed for level of infection against four B. graminis ff.spp, and QTL mapping analyses were performed. Our results demonstrate polygenic inheritance for nonhost resistance, with some QTLs effective only to non-adapted mildews, while others play a role against adapted and non-adapted forms. Histology analyses of nonhost interaction show that most penetration attempts are stopped in association with papillae, and also suggest independent layers of defence at haustorium establishment and conidiophore formation. Nonhost resistance of barley to powdery mildew relies mostly on non-hypersensitive mechanisms. A large-effect nonhost resistance QTL mapped to a 1.4 cM interval is suitable for map-based cloning.
Highlights
Plants are exposed to infinite microorganisms during their lifespan, many of which are potentially harmful
Effector molecules released by the pathogen to undermine PAMP-triggered immunity (PTI) would be perceived by NB-LRRs, triggering a second layer of defence known as effector-triggered immunity (ETI) (Stam et al 2014; Zhang et al 2013)
For B. graminis f.sp. hordei (Bgh) it was not possible to observe any micro-colony on the parents nor on a subset of 50 random Recombinant Inbred Line (RIL), even 14 dai (Online Resource 2a)
Summary
Plants are exposed to infinite microorganisms during their lifespan, many of which are potentially harmful. The evolution of a sophisticated and dynamic immune system has enabled plants to protect themselves against most infectious microorganisms. For a pathogen to be successful in infecting a host plant, it must be adapted to overcome several layers of defence (Jones and Dangl 2006; Nurnberger and Lipka 2005; Thordal-Christensen 2003). Effector molecules released by the pathogen to undermine PTI would be perceived by NB-LRRs, triggering a second layer of defence known as effector-triggered immunity (ETI) (Stam et al 2014; Zhang et al 2013). Schulze-Lefert and Panstruga (2011) hypothesized that, for cases where host and nonhost plant species are phylogenetically closely related, the contribution of ETI to nonhost resistance would be relatively higher than that of PTI There are several examples of the participation of PTI and ETI on nonhost resistance [reviewed in Lee et al (2017)], and, distinction between PAMPs and effectors may not be strict (Thomma et al 2011), it is still an issue whether nonhost resistance relies mainly on PTI or on ETI. Schulze-Lefert and Panstruga (2011) hypothesized that, for cases where host and nonhost plant species are phylogenetically closely related, the contribution of ETI to nonhost resistance would be relatively higher than that of PTI
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