Tomato disease resistances in the post-genomics era

Abstract

Disease in tomato (Solanum lycopersicum) can be caused by many pathogenic organisms, including cellular pathogens (e.g., fungi, bacteria, phytoplasmas, oomycetes and nematodes) and non-cellular pathogens (e.g., viruses and viroids). To respond to pathogen attack, tomato plants, like other sessile organisms, have developed an immune system, where pathogen effectors and plant receptor proteins (e.g., resistance proteins) play a central role. With advances in the genomics era, our understanding of plant-pathogen interactions is evolving rapidly. For example, pathogen genomics has allowed a genome-wide study on the structure, function and evolution of effectors in pathogen genomes. So-called effectoromics offers a high-throughput functional approach to study effector-associated plant genes such as resistance (R) genes and susceptibility (S) genes. In tomato, “genome to germplasms” is facilitating a genome dimension to the exploration of plant diversity in resistance by sequencing and re-sequencing of genomes of available germplasm resources. Together with this breakthrough and powerful techniques for genome editing, novel strategies are being developed for breeding tomatoes with durable resistance to pathogens. Using examples of several tomato diseases, this review focuses on (1) layers of plant immune system, (2) the exploitation of plant S genes in resistance breeding, (3) rapid identification of R and S genes, and (4) novel routes for durable resistance to pathogens. Finally, the topic of breeding for resilience to combined biotic and abiotic stresses is discussed based on our results, which show extensive crosstalk between loci/pathways for resistance to pathogens and tolerance to abiotic stresses.