Cytospora canker, caused by Cytospora mali, is the most destructive disease in production of apples (Malus domestica). Adding potassium (K) to apple trees can effectively control this disease. However, the underlying mechanisms of apple resistance to C. mali under high-K (HK) status remain unknown. Here, we found that HK (9.30 g/kg) apple tissues exhibited high disease resistance. The resistance was impeded when blocking K channels, leading to susceptibility even under HK conditions. We detected a suite of resistance events in HK apple tissues, including upregulation of resistance genes, callose deposition, and formation of ligno-suberized tissues. Further multiomics revealed that the phenylpropanoid pathway was reprogrammed by increasing K content from low-K (LK, 4.30 g/kg) status, leading to increases of 18 antifungal chemicals. Among them, the physiological concentration of coumarin (1,2-benzopyrone) became sufficient to inhibit C. mali growth in HK tissues, and exogenous application could improve the C. mali resistance of LK apple branches. Transgenic apple calli overexpressing beta-glucosidase 40 (MdBGLU40), which encodes the enzyme for coumarin synthesis, contained higher levels of coumarin and exhibited high resistance to C. mali even under LK conditions. Conversely, the suppression of MdBGLU40 through RNAi reduced coumarin content and resistance in HK apple calli, supporting the importance of coumarin accumulation in vivo for apple resistance. Moreover, we found that the upregulation of transcription factor MdMYB1r1 directly activated MdBGLU40 and the binding affinity of MdMYB1r1 to the MdBGLU40 promoter increased in HK apple tissue, leading to high levels of coumarin and resistance in HK apple. Overall, we found that the accumulation of defensive metabolites strengthened resistance in apple when raising K from insufficient to optimal status, and these results highlight the optimization of K content in fertilization practices as a disease management strategy.

Potassium (K) fertilization is crucial for plant resistance to pathogens, but the underlying mechanisms remain unclear. Here, we investigate the molecular mechanism by which the addition of K promotes resistance in Nicotiana benthamiana to Phytophthora parasitica. We found that N. benthamiana with high K content (HK, 52.3 g/kg) produced more ethylene in response to P. parasitica infection, compared to N. benthamiana with low-K content (LK, 22.4 g/kg). An exogenous ethylene application effectively increased resistance in LK N. benthamiana to the level under HK status, demonstrating the involvement of ethylene in the HK-associated resistance in N. benthamiana. Further, transcriptome analysis showed that NbSAMS1, encoding ethylene biosynthesis, was induced to upregulate P. parasitica about five times higher in HK than in LK N. benthamiana. NbSAMS1 overexpression enhanced resistance in LK plants, whereas NbSAMS1 silencing reduced resistance in HK plants, confirming its importance in conferring resistance. Furthermore, we identified a calcium-binding protein, NbCBP1, which interacted with NbSAMS1, promoting its expression in HK N. benthamiana. Silencing NbCBP1 compromised resistance in HK N. benthamiana, whereas its overexpression improved resistance in LK N. benthamiana. Notably, NbCBP1 protected NbSAMS1 from degradation by the 26S proteasome, thereby sustaining ethylene accumulation in HK N. benthamiana in response to P. parasitica infection. Thus, our research elucidated some mechanisms of the NbCBP1-NbSAMS1 module associated with disease resistance in HK N. benthamiana.

Potassium (K) nutrition is a critical determinant of plant disease resistance, but the molecular mechanisms linking K status to defense activation remain unclear. Presently, we systematically investigated the detailed mechanisms by NbVQ1-NbWRKY45-NbCAT2 module in regulating plant immunity under different K statuses. Typically, elevating K content to high (HK, sufficient level) status enhanced pathogen-induced immune responses, particularly reactive oxygen species (ROS) burst, thereby conferring broad-spectrum resistance in Nicotiana benthamiana. Central to this process was the NbVQ1-NbWRKY45-NbCAT2 module, which functioned as a switch for pathogen-triggered ROS burst. In low-K (LK) plants, NbWRKY45 was upregulated through a self-amplifying loop, thereby inducing NbCAT2 expression to scavenge ROS and ultimately compromising plant disease resistance. In contrast, adding K promoted NbVQ1 expression, which proved essential for the K-enhanced plant resistance. NbVQ1 interacted with the WRKYGQK domain of NbWRKY45 through its VQ motif, thereby disrupting the binding affinity of NbWRKY45 to NbCAT2 promoter and causing NbCAT2 downregulation. This transcriptional suppression of NbCAT2 resulted in stronger ROS bursts and improved the resistance of N. benthamiana to Botrytis cinerea and Phytophthora parasitica under HK status. Notably, K+ could promote the interaction between NbVQ1 and NbWRKY45, directly explicating nutrient-associated immune potentiation mechanism. Moreover, this K-dependent resistance mechanism mediated by VQ1-WRKY45-CAT2 module was conserved in Arabidopsis thaliana, while suppression of NbWRKY45 also increased plant drought tolerance. Overall, this study established the VQ-WRKY-CAT module as a molecular switch for K-promoted ROS immunity and provided mechanistic evidence for coupling K nutrition with transcriptional regulation of plant immunity.

Anthracnose, caused by Colletotrichum musae, is the most devastating postharvest disease limiting the shelf life and marketability of banana fruit. While γ-aminobutyric acid (GABA) is known to mitigate abiotic stress, its role and mechanisms in controlling postharvest diseases remain elusive. Here, we report that exogenous GABA treatment significantly attenuates anthracnose severity in harvested banana fruit. Through integrative physiological and transcriptomic analyses, we identified a non-specific lipid transfer protein, MaLTP60, as a critical regulator robustly triggered by GABA signaling and C. musae challenge. Crucially, silencing of MaLTP60 attenuated GABA-induced disease resistance. Then, we demonstrate that MaLTP60 orchestrates a dual-mechanism antioxidant defense to maintain redox homeostasis. Mechanistically, MaLTP60 physically targets the mitochondrial voltage-dependent anion channel MaVDAC9. Structural modeling and functional assays reveal that MaLTP60 acts as a molecular plug to occlude the MaVDAC9 pore, thereby blocking ROS transport, inhibiting channel activity and antagonizing MaVDAC9-mediated susceptibility. Concurrently, MaLTP60 interacts with the peroxiredoxin MaPRDX1 and functions as an affinity helper, synergistically enhancing its stabilization and ROS-scavenging efficiency. Collectively, our findings uncover a novel regulatory network in which GABA-induced MaLTP60 functions as a redox brake that coordinates dual antioxidant strategies to confer basal immunity in banana fruit to C. musae.