Resistance to turnip crinkle virus in Arabidopsis is regulated by two host genes and is salicylic acid dependent but NPR1, ethylene, and jasmonate independent.

Inoculation of turnip crinkle virus (TCV) on the resistant Arabidopsis ecotype Dijon (Di-17) results in the development of a hypersensitive response (HR) on the inoculated leaves. To assess the role of the recently cloned HRT gene in conferring resistance, we monitored both HR and resistance (lack of viral spread to systemic tissues) in the progeny of a cross between resistant Di-17 and susceptible Columbia plants. As expected, HR development segregated as a dominant trait that corresponded with the presence of HRT. However, all of the F(1) plants and three-fourths of HR(+) F(2) plants were susceptible to the virus. These results suggest the presence of a second gene, termed RRT, that regulates resistance to TCV. The allele present in Di-17 appears to be recessive to the allele or alleles present in TCV-susceptible ecotypes. We also demonstrate that HR formation and TCV resistance are dependent on salicylic acid but not on ethylene or jasmonic acid. Furthermore, these phenomena are unaffected by mutations in NPR1. Thus, TCV resistance requires a yet undefined salicylic acid-dependent, NPR1-independent signaling pathway.