The impacts of high temperature on bacterial blight resistance genes in rice

Abstract

Rice is cultivated around the world and serves as a primary source of income and calories for many people. However, rice yield is threatened by the bacteria Xanthomonas oryzae pv. oryzae (Xoo), and outbreaks can be devastating to global communities. Xoo is the causal agent of bacterial blight (BB) in rice, and it proliferates in rice-growing climates. As climate change progresses, the trend of increasing BB severity may result in increased losses for growers. Disease severity, quantified through lesion lengths, increases at high temperature in rice. Previous studies indicated this pattern of increased disease phenotypes occurs even when a resistance (R) gene is present, except for one, Xa7. Our rationale for these experiments is to determine if the classification of an R gene can predict its performance against BB outbreaks. The classification of R genes in rice is a recent addition to the scope of our knowledge of plant pathology and has been the result of studies on nucleotide polymorphisms, genetic mapping, and fluorescent imaging of protein localization. Grouping the underlying mechanisms of action of individual R genes, such as the executor genes Xa7 and Xa10, allow for comparative studies to further elucidate details of their assigned classes. Not all R genes have been classified, but establishing a trend that some R genes maintain efficacy under higher temperatures would provide breeders with more tools to develop climate-friendly rice lines. This study indicates that R genes that remain effective at high temperature may be classified into the same category of executor R genes. More research is needed to determine if R gene classification predicts durability under heat stress. This study explores BB lesion lengths and Xoo colony counts at high and low temperatures. We find that at high temperature relative to low temperature, disease lesions were more severe in IR24, containing no active R gene, and in plants containing the R genes Xa21, xa5, and Xa3. Lesions were shorter in plants with Xa7 and Xa10. Additionally, under the same treatments, bacterial numbers increased to higher levels in IR24, Xa21, xa5, and Xa3. Numbers in Xa7 were reduced while numbers in Xa10 were low early in infection, but eventually increased beyond those measured at low temperature. Degree of lesion restriction did not always correspond to degree of restricted bacterial numbers, suggesting that severity of lesions may not always be a predictor of bacterial multiplication in the plant. Xa7 and Xa10 are classified as executor R genes. The mechanism of action in these genes may play a role in their durability at high temperatures. We hypothesize that the success of executor R genes may be a result of protein accumulation in the nucleus. This mechanism might be analogous to instances of temperature sensitive pathogen defense related protein accumulation, as seen in Arabidopsis. This mechanism may be induced or enhanced by the presence of reactive oxygen species (ROS) or other heat-stress related markers. More research is needed to explore the signaling between heat-stress pathways and R genes.