Abstract
Summary Candidate effectors from lettuce downy mildew (Bremia lactucae) enable highâthroughput germplasm screening for the presence of resistance (R) genes. The nonhost species Lactuca saligna comprises a source of B. lactucae R genes that has hardly been exploited in lettuce breeding. Its crossâcompatibility with the host species L. sativa enables the study of inheritance of nonhost resistance (NHR).We performed transient expression of candidate RXLR effector genes from B. lactucae in a diverse Lactuca germplasm set. Responses to two candidate effectors (BLR31 and BLN08) were genetically mapped and tested for coâsegregation with disease resistance.BLN08 induced a hypersensitive response (HR) in 55% of the L. saligna accessions, but responsiveness did not coâsegregate with resistance to Bl:24. BLR31 triggered an HR in 5% of the L. saligna accessions, and revealed a novel R gene providing complete B. lactucae race Bl:24 resistance. Resistant hybrid plants that were BLR31 nonresponsive indicated other unlinked R genes and/or nonhost QTLs.We have identified a candidate avirulence effector of B. lactucae (BLR31) and its cognate R gene in L. saligna. Concurrently, our results suggest that R genes are not required for NHR of L. saligna.
Highlights
Nonhost resistance (NHR) is defined as immunity occurring in all genotypes of a plant species against all genotypes of a specific pathogen (Heath, 1981; Niks, 1987; Niks & Marcel, 2009)
Two B. lactucae candidate effectors trigger an hypersensitive response (HR) in L. saligna accessions
Sixteen candidate effectors with RXLR(-like) motifs were predicted from newly generated B. lactucae transcriptome data and could be added to the 34 published previously (Stassen et al, 2012)
Summary
Nonhost resistance (NHR) is defined as immunity occurring in all genotypes of a plant species against all genotypes of a specific pathogen (Heath, 1981; Niks, 1987; Niks & Marcel, 2009). Understanding the mechanisms of NHR may lead to the development of durable and broad-spectrum disease resistance in crop plants. The first layer depends on the recognition of pathogen-derived molecules, called pathogen-associated molecular patterns (PAMPs). PAMP recognition, commonly through pattern recognition receptors, can lead to resistance and is referred to as PAMP-triggered immunity (PTI). To counteract PTI, pathogens secrete effector molecules targeting host intracellular compartments that enhance infection through the manipulation of host cellular processes, leading to effector-triggered susceptibility (ETS)
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