Rme1 is necessary for Mi-1-mediated resistance and acts early in the resistance pathway

The tomato gene Mi-1 confers resistance to root-knot nematodes (Meloidogyne spp.), potato aphid, and whitefly. Using genetic screens, we have isolated a mutant, rme1 (resistance to Meloidogyne spp.), compromised in resistance to M. javanica and potato aphid. Here, we show that the rmel mutant is also compromised in resistance to M. incognita, M. arenaria, and whitefly. In addition, using an Agrobacte-Hum-mediated transient assay in leaves to express constitutive gain-of-function mutant Pto(L205D), we demonstrated that the rmel mutation is not compromised in Pto-mediated hypersensitive response. Moreover, the mutation in rmel does not result in increased virulence of pathogenic Pseudomonas syringae or Mi-1-virulent M. incognita. Using a chimeric Mi-1 construct, Mi-DS4, which confers constitutive cell death phenotype and A. rhizogenes root transformation, we showed that the Mi-1-mediated cell death pathway is intact in this mutant. Our results indicate that Rme1 is required for Mi-1-mediated resistance and acts either at the same step in the signal transduction pathway as Mi-1 or upstream of Mi-1.