ABSTRACT
Several accessions of Nicotiana langsdorffii, a wild tobacco relative native to South America, express an incompatible interaction in response to infection by Peronospora tabacina, an oömycete that causes blue mold disease of tobacco (N. tabacum) and many other species of Nicotiana. In resistant accessions of N. langsdorffii, such as S-4-4, incompatibility takes the form of necrotic lesions that appear 48 h after pathogen inoculation, restricting pathogen growth, and suppressing subsequent asexual sporulation. Significantly elevated levels of salicylic acid and expression of a defense-related gene (HSR203J) were observed in S-4-4 leaves following blue mold infection. Genetic segregation analysis in F(2) and modified backcross populations showed that blue mold resistance is determined by a single dominant gene (NlRPT) present in S-4-4. Further characterization of this unique host-pathogen interaction has revealed that (i) necrotic lesion resistance is due to the hypersensitive response (HR), (ii) HR-mediated resistance is present in 7 of 10 N. langsdorffii accessions examined, but not in closely related species, (iii) in some accessions of N. langsdorffii, resistance is expressed in cotyledon tissue and seedling leaves as well as in adult plants, and (iv) several resistant accessions including S-4-4 express an unregulated ("runaway") HR in response to P. tabacina infection.