The Mi-9 gene from Solanum arcanum conferring heat-stable resistance to root-knot nematodes is a homolog of Mi-1.

Resistance conferred by the Mi-1 gene from Solanum peruvianum is effective and widely used for limiting root-knot nematode (Meloidogyne spp.) yield loss in tomato (Solanum lycopersicum), but the resistance is ineffective at soil temperatures above 28 degrees C. Previously, we mapped the heat-stable resistance gene Mi-9 in Solanum arcanum accession LA2157 to the short arm of chromosome 6, in a genetic interval as Mi-1 and the Cladosporium fulvum resistance gene Cf2. We developed a fine map of the Mi-9 region by resistance and marker screening of an F2 population and derived F3 families from resistant LA2157 x susceptible LA392. Mi-1 intron 1 flanking primers were designed to amplify intron 1 and fingerprint Mi-1 homologs. Using these primers, we identified seven Mi-1 homologs in the mapping parents. Cf-2 and Mi-1 homologs were mapped on chromosome 6 using a subset of the F2. Cf-2 homologs did not segregate with Mi-9 resistance, but three Mi-1 homologs (RH1, RH2, and RH4) from LA2157 and one (SH1) from LA392 colocalized to the Mi-9 region. Reverse transcriptase-polymerase chain reaction analysis indicated that six Mi-1 homologs are expressed in LA2157 roots. We targeted transcripts of Mi-1 homologs for degradation with tobacco (Nicotiana tabacum) rattle virus (TRV)-based virus-induced gene silencing using Agrobacterium infiltration with a TRV-Mi construct. In most LA2157 plants infiltrated with the TRV-Mi construct, Mi-9-mediated heat-stable root-knot nematode resistance was compromised at 32 degrees C, indicating that the heat-stable resistance is mediated by a homolog of Mi-1.

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 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 Pto(L205D), 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.

Aphid-induced defense responses in Mi-1-mediated compatible and incompatible tomato interactions.

The tomato Mi-1 gene confers resistance to three species of root-knot nematode and potato aphid. We studied changes in expression of jasmonic acid (JA)- and salicylic acid (SA)-dependent defense genes in response to potato and green peach aphids. We determined changes in three PR proteins, lipoxygenase and proteinase inhibitors I and II transcripts, locally and systemically in both compatible and incompatible interactions in tomato. Transcripts for PR-1 were detected earlier and accumulated to higher levels in the incompatible than in the compatible potato aphid/tomato interactions. The transcript profiles of the other genes were similar in compatible compared with incompatible interactions. Pin1 and Pin2 RNAs were detected early and transiently in both compatible and incompatible interactions. In tomato plants containing Mi-1, systemic expression of PR-1 and GluB was detected in both compatible and incompatible interactions at 48 h after infestations with either aphid. These results suggest that aphid feeding involves both SA and JA/ethylene plant defense signaling pathways and that Mi-1-mediated resistance might involve a SA-dependent signaling pathway. Potato aphid feeding generated reactive oxygen species in both compatible and incompatible interactions. However, a hypersensitive response was absent in the Mi-1-mediated resistance response to potato aphids. Reciprocal grafting experiments revealed that resistance is cell autonomous, and local expression of Mi-1 is required for Mi-1-mediated resistance against the potato aphid.