Fig. 7

Summary model of the metabolic processes underlying the response of K-starved rice to S. oryzae infection. First, S. oryzae invades rice from FLSs and causes H₂O₂ accumulation, which results in severe oxidative stress. However, MGDG and DGDG contents, which are essential for maintaining membrane integrity and stability, were profoundly decreased in the K-starved FLSs. Likewise, K deficiency also decreases the synthesis of the antioxidant glutathione and the activities of SOD and POD. The consistent accumulation of H₂O₂ in K-starved rice induces lipid peroxidation, which accelerates 1-alkyl-2-acylglycerophosphoethanolamine and linoleic acid accumulation in K-starved FLSs. Second, S. oryzae infection impacts the biosynthesis of aminoacyl-tRNA, which results in amino acid accumulation in FLSs. Proline is upregulated and citrate is downregulated in K-starved rice, implying that energy metabolism and osmotic balance are disrupted by S. oryzae infection. As a systematic response, S. oryzae infection also induces the degradation of chloroplasts in flag leaves, which down regulates the photosynthetic rate of K-starved rice. Overall, alterations in these series of metabolic processes in K-starved rice promote S. oryzae development and sheath rotting. Note: FC in metabolite abundance for the treatments versus controls was calculated. The log₂(FC) is indicated by the shade of red or blue according to the color scale, and the numbers below the rectangle indicate the corresponding log₂(FC) values. The metabolites or physiological parameters in red/blue represent up/down regulation in − K + I-treated plants versus + K + I-treated plants. The symbol “?” means that the mechanism is not yet clear