Root-knot nematodes (RKNs) are obligate plant parasites causing major economic damage to many crops including tomato. These nematodes have evolved a complex and intimate relationship with their hosts. This communication is highly specific, suggesting that the plant nematode interactions involve a continual exchange of signals between the two organisms. Initiation of pathogenic interaction depends on the nematode ability to recognize, penetrate, and initiate an elaborate feeding site. Plants have evolved effective mechanisms to recognize pathogens and to stop their growth. A common mechanism of race-specific resistance to a large number of pathogens, including nematodes, is the induction of hypersensitive response (HR) or cell death.

The tomato gene, Mi-1, is the first cloned plant resistance gene with dual specificity to two unrelated organisms, a nematode and an aphid. Despite this novel function, Mi-1 encodes a protein sharing molecular features, nucleotide binding site and leucine rich repeats, with described single-specificity resistance genes. Resistance to nematodes is characterized by HR in roots, however no HR is detected in leaves in the Mi-1-mediated resistance to the potato aphid. We are employing both genetic and molecular approaches to dissect the Mi-1-mediated resistance pathway to both organisms. We are using mutational analysis to identify and characterize plant genes that are required for nematode and aphid recognition and the subsequent expression of resistance. We have identified a gene Rme1 (for resistance to Meloidogyne), that is required for both nematode and aphid resistance. Recent experiments indicated that Rme1 acts early in the Mi-1 resistance signal transduction pathway, either at the Mi-1 level or before Mi-1. We are also using microarray analysis to study aphid and nematode feeding responses in resistant and susceptible tomato.