Location: Vegetable Crops Research Unit
Title: Phenotypic characterization of potato late blight resistance mediated by the broad-spectrum resistance gene RB Authors
|Chen, Yu -|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 25, 2010
Publication Date: February 1, 2011
Citation: Chen, Y., Halterman, D.A. 2011. Phenotypic characterization of potato late blight resistance mediated by the broad-spectrum resistance gene RB. Phytopathology. 101(2):263-270. Interpretive Summary: The potato late blight resistance (R) gene RB is distinct from most plant R genes in that it confers resistance to a broad spectrum of pathogen isolates. It also confers partial resistance instead of immunity to late blight. In this manuscript we describe the resistance phenotype mediated by RB. Through comparison with the isolate-specific R gene R9, we have found that RB mediates the induction of host responses similar to isolate-specific genes but that the partial resistance phenotype is likely due to the timing and intensity of these responses. While RB-containing plants are still considered resistant, they allow the pathogen to spread beyond the initial site of inoculation. These research results will impact potato breeders interested in incorporating RB-mediated resistance into their breeding materials.
Technical Abstract: Potato late blight, caused by oomycete pathogen Phytophthora infestans (Mont.) de Bary, is one of the most destructive plant diseases worldwide. One of the best ways to control this disease is through genetically determined resistance. A isolate-nonspecific resistance gene RB, cloned from the wild potato species S. bulbocastanum, exhibits partial resistance to a broad-spectrum of P. infestans isolates. Here, we have compared host resistance responses mediated by RB with the isolate-specific resistance gene R9. Through examination of hypersensitive cell death response (HR) induction in potato with RB or R9, we found that both genes can elicit the HR. However, in plants with RB the pathogen escaped HR lesions and continued to grow beyond inoculation sites. These results suggest that RB may use molecular mechanisms similar to race-specific R genes, but responses do not completely stop pathogen spread. Callose deposition was negatively correlated with resistance levels in RB, R9, and susceptible plants. We also monitored the transcription of pathogenesis related (PR) genes PR-1 basic, PR-2, PR-5, and the HR-associated gene HIN1 after P. infestans inoculation. Transcription patterns of these genes suggest differences in intensity and timing of responses mediated by race-specific and race-nonspecific resistance genes.