Abstract
BackgroundBakanae disease, caused by the fungus Fusarium fujikuroi, occurs widely throughout Asia and Europe and sporadically in other rice production areas. Recent changes in climate and cropping patterns have aggravated this disease. To gain a better understanding of the molecular mechanisms of rice bakanae disease resistance, we employed a 6-plex tandem mass tag approach for relative quantitative proteomic comparison of infected and uninfected rice seedlings 7 days post-inoculation with two genotypes: the resistant genotype 93–11 and the susceptible genotype Nipponbare.ResultsIn total, 123 (77.2% up-regulated, 22.8% down-regulated) and 91 (94.5% up-regulated, 5.5% down-regulated) differentially expressed proteins (DEPs) accumulated in 93–11 and Nipponbare, respectively. Only 11 DEPs were both shared by the two genotypes. Clustering results showed that the protein regulation trends for the two genotypes were highly contrasting, which suggested obviously different interaction mechanisms of the host and the pathogen between 93 and 11 and Nipponbare. Further analysis showed that a noticeable aquaporin, PIP2–2, was sharply upregulated with a fold change (FC) of 109.2 in 93–11, which might be related to pathogen defense and the execution of bakanae disease resistance. Certain antifungal proteins were regulated in both 93–11 and Nipponbare with moderate FCs. These proteins might participate in protecting the cellular integrity required for basic growth of the susceptible genotype. Correlation analysis between the transcriptome and proteome revealed that Pearson correlation coefficients of R = 0.677 (P = 0.0005) and R = − 0.097 (P = 0.702) were obtained for 93–11 and Nipponbare, respectively. Our findings raised an intriguing result that a significant positive correlation only in the resistant genotype, while no correlation was found in the susceptible genotype. The differences in codon usage was hypothesized for the cause of the result.ConclusionsQuantitative proteomic analysis of the rice genotypes 93-11and Nipponbare after F. fujikuroi infection revealed that the aquaporin protein PIP2–2 might execute bakanae disease resistance. The difference in the correlation between the transcriptome and proteome might be due to the differences in codon usage between 93-11and Nipponbare. Overall, the protein regulation trends observed under bakanae disease stress are highly contrasting, and the molecular mechanisms of disease defense are obviously different between 93 and 11 and Nipponbare. In summary, these findings deepen our understanding of the functions of proteins induced by bakanae disease and the mechanisms of rice bakanae disease resistance.
Highlights
Bakanae disease, caused by the fungus Fusarium fujikuroi, occurs widely throughout Asia and Europe and sporadically in other rice production areas
The results revealed that certain WRKYs, WAK and MAP3Ks were responsible for the bakanae disease resistance of 93-11and showed that the defense-related genes (WRKYs and MARKs) on chromosome 1 that are modulated in 93–11 upon infection might play a crucial role in the rice-F. fujikuroi interaction
Hur et al [7] used the resistant indica variety Shingwang and the susceptible japonica variety Ilpum to generateNILs for identifying Quantitative trait loci (QTLs) associated with bakanae disease resistance
Summary
Bakanae disease, caused by the fungus Fusarium fujikuroi, occurs widely throughout Asia and Europe and sporadically in other rice production areas. Rice (Oryza sativa L.) is one of the world’s most important food crops, serving as a staple for more than 50% of the world population. In China, rice is a staple food crop that feeds more than 60% of the population and contributes nearly 40% of the total calorie intake [1]. Many diseases play an important role in determining the yield and cost of food. Rice bakanae disease, caused by the fungus Fusarium fujikuroi, is an important disease in rice. Bakanae disease occurs widely throughout Asia and Europe, and sporadically in other areas of rice production [3, 4]. Bakanae disease can be managed to a certain extent using chemical fungicides [5] through seed treatment and soil amendment, a more efficient, sustainable and environmentally friendly solution is to explore genetic resources that are resistant to the disease and breed additional high-resistance genotypes
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