Understanding The Interactions Between Plants And Pathogens Using Infection Of Tomato (Solanum Lycopersicum) By Phytophthora Infestans As A Model Pathosystem

The oomycete Phytophthora infestans causes devastating epidemics for both tomato (Solanum lycopersicum) and potato (Solanum tuberosum) worldwide (Fry 2008). There is a limited understanding of the mechanisms by which P. infestans overcomes plant defenses and how it regulates its pathogenicity factors; behaving as a biotroph during early stages of infection and switching to a necrotroph at later stages. To address these limitations, 454 sequencing was used to learn about the transcriptome of P. infestans (US-11 clonal lineage) in a compatible interaction with its host tomato (Solanum lycopersicum cv. M82), at three infection stages: biotrophic, the transition from biotrophy to necrotrophy and necrotrophic phase. This approach identified more than 550,000 high quality sequence reads, of which about 10% were derived from P. infestans. The tomato and P. infestans transcriptomes provided a comprehensive overview of the molecular interaction between plants and pathogens. On the host side, nearly 12,000 genes showed differential expression during the three infection stages analyzed. These genes corresponded to nearly 200 biochemical pathways, revealing a massive reorganization of the plant metabolism. Amongst these, probable components of resistance were up-regulated. For example, more than 100 putative resistance genes and more than 100 putative Pattern Recognition Receptor (PRRs) genes were induced. Transcript abundance of genes encoding proteins in the SA pathway increased in the biotrophic phase, and subsequently declined. In contrast, transcript abundance of genes in the JA pathway gradually increased as infection progressed. The expression of nearly 9,000 P. infestans genes was detected throughout the interaction. Of these, 800 had not been identified previously in the P. infestans genome. Many genes, including effectors, were stage-specific. It was determined that five candidate effector genes (three RXLRs, one CRN and one hypothetical protein), suppressed necrosis caused by the P. infestans necrosis inducing protein PiNPP1.1 suggesting that these effectors might prolongue the biotrophic phase of P. infestans. In addition, a model pathosystem (Hyaloperonospora arabidopsidis infection of Arabidopsis thaliana) was used to investigate the genetic basis and the mechanisms of action of quantitative resistance. Two putative quantitative resistant loci (QRL) were found, of which one is likely an R gene, but the other may be a quantitative resistance locus. The nature of this QRL awaits investigation