Comparison of defense responses of transgenic potato lines expressing three different Rpi genes to specific Phytophthora infestans races based on transcriptome profiling.

Potato late blight, one of the most devastating diseases in potato, is caused by the oomycete Phytophthora infestans. Over 20 resistance genes have been cloned including R1, R3a, and R3b. The distinctions between defense response mechanisms mediated by different resistance genes are still unclear. Here we performed transcriptome profiling in three transgenic lines, R1, R3a, and R3b, and wild-type Desiree under inoculation with two P. infestans isolates, 89148 (race 0) and CN152 (super race), using RNA-seq. Compared with wild type, specific differentially expressed genes (DEGs) were identified in the three transgenic lines. The highest number of DEGs occurred in transgenic R3b, with 779 DEGs in response to isolate 89148 and 864 DEGs in response to infection by CN152, followed by transgenic R1 lines with 408 DEGs for isolate 89148 and 267 DEGs for CN152. Based on gene ontology, the most common GO terms (15 for 89148 and 20 for CN152) were enriched in transgenic R3a and R3b lines. This indicates that the defense pathways mediated by R3a and R3b are more similar than those mediated by R1. Further separate GO analysis of up- or down-regulated DEGs showed that the down-regulated DEGs mainly functioned in mediating the resistance of potato to P. infestans 89148 by response to stress biological process and to CN152 by oxidation reduction biological process. KEGG pathways of DNA replication, plant-pathogen interaction and pentose and glucuronate interconversions are unique for transgenic R1, R3a, and R3b lines in incompatible interactions. Quantitative real-time PCR experimental validation confirmed the induced expression of DEGs in the late blight resistance signaling pathway. Our results will lay a solid foundation for further understanding the mechanisms of plant-pathogen interactions, and provide a theoretical reference for durable resistance in potato.