The crosstalk between brassinosteroid (BR) and jasmonic acid (JA) signaling is crucial for plant growth and defense responses. However, the detailed interplay between BRs and JA remains obscure. Here, we found that the rice (Oryza sativa) Glycogen synthase kinase3 (GSK3)-like kinase OsGSK2, a conserved kinase serving as a key suppressor of BR signaling, enhanced antiviral defense and the JA response. We identified a member of the JASMONATE ZIM-domain (JAZ) family, OsJAZ4, as a OsGSK2 substrate and confirmed that OsGSK2 interacted with and phosphorylated OsJAZ4. We demonstrated that OsGSK2 disrupted the OsJAZ4-OsNINJA complex and OsJAZ4-OsJAZ11 dimerization by competitively binding to the ZIM domain, perhaps helping to facilitate the degradation of OsJAZ4 via the 26S proteasome pathway. We also showed that OsJAZ4 negatively modulated JA signaling and antiviral defense and that the BR pathway was involved in modulating the stability of OsJAZ4 protein in an OsCORONATINE INSENSITIVE1-dependent manner. Collectively, these results suggest that OsGSK2 enhances plant antiviral defenses by activating JA signaling as it directly interacts with, phosphorylates, and destabilizes OsJAZ4. Thus, our findings provide a clear link between BR and JA signaling.

The functions of microRNA156 (miR156) and its targeted SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) transcription factor genes in plant development have been widely investigated. However, the role of the miR156/SPLs regulatory network in plant immune systems remains obscure. Here, we found that the accumulation of reactive oxygen species (ROS) and the transcripts of basal salicylic acid (SA) signaling pathway genes were lower in Arabidopsis Pro35S:MIR156 seedlings (miR156 overexpression mutants) but higher in Pro35S:MIM156 (miR156 repression mutants) and ProSPL9:rSPL9 (SPL9 overexpression mutants) seedlings compared with wild-type Col-0 plants (WT). As a result, Pro35S:MIR156 mutants induced greater susceptibility to Pseudomonas syringae pv. tomato DC3000 following syringe infiltration than WT, while Pro35S:MIM156 and ProSPL9:rSPL9 mutants showed enhanced resistance. In addition, foliar H2O2 application resulted in activation of SA-mediated defense response and ablation of miR156-induced susceptibility to P. syringae pv. tomato DC3000 infection. Collectively, our results provide new insights into the function of the miR156/SPL network in Arabidopsis immune response by regulating ROS accumulation and activating the SA signaling pathway.

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Phosphate (Pi) and MYC2‐mediated jasmonate (JA) pathway play critical roles in plant growth and development. In particular, crosstalk between JA and Pi starvation signalling has been reported to mediate insect herbivory resistance in dicot plants. However, its roles and mechanism in monocot‐bacterial defense systems remain obscure. Here, we report that Pi starvation in rice activates the OsMYC2 signalling and enhances resistance to Xanthomonas oryzae pv. oryzae (Xoo) infection. The direct regulation of OsPHR2 on the OsMYC2 promoter was confirmed by yeast one‐hybrid, electrophoretic mobility shift, dual‐luciferase and chromatin immunoprecipitation assays. Molecular analyses and infection studies using OsPHR2‐Ov1 and phr2 mutants further demonstrated that OsPHR2 enhances antibacterial resistance via transcriptional regulation of OsMYC2 expression, indicating a positive role of OsPHR2‐OsMYC2 crosstalk in modulating the OsMYC2 signalling and Xoo infection. Genetic analysis and infection assays using myc2 mutants revealed that Pi starvation‐induced OsMYC2 signalling activation and consequent Xoo resistance depends on the regulation of OsMYC2. Together, these results reveal a clear interlink between Pi starvation‐ and OsMYC2‐ signalling in monocot plants, and provide new insight into how plants balance growth and defence by integrating nutrient deficiency and phytohormone signalling. We highlighted a molecular link connecting OsMYC2‐mediated JA pathway and phosphate starvation signalling in monocot plant. We demonstrated that phosphate starvation promoted OsMYC2 signalling to enhance rice defence to bacterial blight via transcriptional regulation of OsPHR2 on OsMYC2.