| Root-knot nematode (RKN: Meloidogyne spp.) is a major crop pathogen worldwide, but is very difficult to manage. Effective host resistance exists for a few plant species, including that conditioned by the Mi gene in tomato (Solanum lycopersicum). I interrogated the root transcriptome of the resistant (Mi+) and susceptible (Mi-) cultivars Motelle and Moneymaker respectively during a time-course infection by the Mi-susceptible RKN species, M. incognita, and the Mi-resistant species, M. hapla. In the absence of RKN infection, only a single significantly regulated gene, encoding a glycosyltransferase, was detected. However, RKN infection influenced the expression of broad suites of genes; more than half of the probes on the array identified differential gene regulation between infected and uninfected root tissue at some stage of RKN infection. I discovered 217 genes regulated during the time of RKN infection corresponding to establishment of feeding sites, and 58 genes that exhibited differential regulation in resistant roots compared to uninfected roots, including the glycosyltransferase. Using VIGS to silence the expression of this gene restored susceptibility to Meloidogyne incognita in Motelle, indicating that this gene is necessary for resistance to RKN. Collectively, these data provide a picture of global gene expression changes in roots during compatible and incompatible associations with RKN, and point to candidates for further investigation. These data, combined with a thorough annotation and characterization of 186 transcripts sequenced from an RKN feeding site tissue specific EST library provide a comprehensive report on gene expression changes in tomato during RKN infection.; In addition to exploring host responses to RKN, I examined gene regulation in nematodes during pathogenesis and demonstrated that both nematode transcripts and changes in expression can be detected using labeled RNA extracted from infected root tissue, saving time and resources by alleviating the need to dissect out the nematodes.; The results reported herein expand our knowledge of both host and nematode gene expression regulation during a sophisticated parasitic interaction. |