Background
Bakanae 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.
Conclusions
Quantitative 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.
Results
In 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. Conclusions: Quantitative 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.