Basal Differences in the Transcriptional Profiles of Tomato Roots Associated with the Presence/Absence of the...

The Mi-1 gene of tomato is responsible for the resistance of certain genotypes to root-knot nematodes or RKN (Meloidogyne spp.) and other harmful organisms such as aphids or whiteflies, in a complex cascade of transcriptional changes in which other tomato genes are also involved. The objective of this study was to gain a deeper understanding of the Mi-1-mediated resistance of tomato to Meloidogyne javanica using oligonucleotide microarrays to identify additional plant genes involved in the compatible or incompatible tomato/nematode interactions. Microarray analysis was selected as it has been widely used to identify genes involved in plant resistance to pests and pathogens. In a first phase of the present work, the roots of uninfested tomato plants were analyzed, comparing the transcriptional profiles of susceptible (Moneymaker) and resistant (Motelle) cultivars. In Motelle, 180 transcripts were more expressed than in Moneymaker and only 44 transcripts showed lower expression. Motelle showed higher activity in salicylic, jasmonic and ethylene pathways, while the GAI protein was strongly repressed compared to Moneymaker. These and other basal differences provided valuable information on candidate genes associated with the presence of the Mi-1 gene in Motelle. Subsequent infection by M. javanica triggered an intense transcriptional reprograming that increased over time throughout both compatible (Moneymaker) and incompatible (Motelle) interactions, with scarce genes common to both interactions. At the early phase of infection (2 dpi), genes for the cell wall, hormones, RNA, stress, and transport were up-regulated in the compatible interaction, and signaling, protein, and redox genes were down-regulated; in the incompatible interaction, protease inhibitors were up-regulated, and hormone and RNA genes were down-regulated. Later (12 dpi), genes for hormones, the cell wall, RNA, stress, defense, and development were up-regulated in the compatible interaction, while transport and some stress/defense genes were down-regulated; the incompatible interaction showed mixed regulation within hormone, stress, and defense genes.