Hypersensitivity to triforine in lettuce is triggered by a TNL gene through the disease-resistance pathway.

Abstract

The majority of cloned disease resistance genes (R-genes) encode proteins with nucleotide-binding leucine-rich repeat domains (NLRs). R-genes tend to be physically clustered, and the structure of the cluster often facilitates expansion and sequence exchange among R-gene homologs (Luo et al. 2012). NLR proteins interact directly or indirectly with pathogens effectors, often triggering programmed cell death, also known as hypersensitive response (HR) at the infected sites (Dangl and Jones 2001). HR may be triggered by pesticide molecules rather than pathogen effectors. For example, some tomato cultivars are sensitive to fenthion, developing toxic lesions after exposure to fenthion (Martin et al. 1994). Similarly, some lettuce germplasms are highly sensitive to triforine, an active ingredient in some commercial fungicides, with leaves showing wilting and necrosis 24 hours after exposure to triforine (Figure 1a). Sensitivity to triforine in lettuce is controlled by a single locus (Tr) (Simko et al. 2011), however, the causal gene and its molecular mechanism remain unknown.