Rme1 is Specific for Mi-1-Mediated Resistance and Acts Early in the Resistance Pathway

Abstract

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) compromised in resistance to M. javanica and potato aphid. Here we show that the rme1 mutant is also compromised in resistance to M. incognita, M. arenaria and whitefly. In addition, using an Agrobacterium-mediated transient assay in leaves to express constitutive gain-of-function mutant PtoL205D, we demonstrated that the rme1 mutation is not compromised in Pto-mediated hypersensitive response. Moreover, the mutation in rme1 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.