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Summary: Brown planthopper (BPH, Nilaparvata lugens), a highly destructive insect pest, poses a serious threat to rice (Oryza sativa) production worldwide. Jasmonates are key phytohormones that regulate plant defences against BPH; however, the molecular link between jasmonates and BPH responses in rice remains largely unknown. Here, we discovered a Poaceae‐specific metabolite, mixed‐linkage β‐1,3;1,4‐d‐glucan (MLG), which contributes to jasmonate‐mediated BPH resistance. MLG levels in rice significantly increased upon BPH attack. Overexpressing OsCslF6, which encodes a glucan synthase that catalyses MLG biosynthesis, significantly enhanced BPH resistance and cell wall thickness in vascular bundles, whereas knockout of OsCslF6 reduced BPH resistance and vascular wall thickness. OsMYC2, a master transcription factor of jasmonate signalling, directly controlled the upregulation of OsCslF6 in response to BPH feeding. The AT‐rich domain of the OsCslF6 promoter varies in rice varieties from different locations and natural variants in this domain were associated with BPH resistance. MLG‐derived oligosaccharides bound to the plasma membrane‐anchored LECTIN RECEPTOR KINASE1 OsLecRK1 and modulated its activity. Thus, our findings suggest that the OsMYC2‐OsCslF6 module regulates pest resistance by modulating MLG production to enhance vascular wall thickness and OsLecRK1‐mediated defence signalling during rice‐BPH interactions. [ABSTRACT FROM AUTHOR]

Immune response in plants is tightly regulated by the coordination of the cell surface and intracellular receptors. In animals, the membrane attack complex/perforin-like (MACPF) protein superfamily creates oligomeric pore structures on the cell surface during pathogen infection. However, the function and molecular mechanism of MACPF proteins in plant pathogen responses remain largely unclear. In this study, we identified an Arabidopsis MACP2 and investigated the responsiveness of this protein during both bacterial and fungal pathogens. We suggest that MACP2 induces programmed cell death, bacterial pathogen resistance, and necrotrophic fungal pathogen sensitivity by activating the biosynthesis of tryptophan-derived indole glucosinolates and the salicylic acid signaling pathway dependent on the activity of enhanced disease susceptibility 1 (EDS1). Moreover, the response of MACP2 mRNA isoforms upon pathogen attack is differentially regulated by a posttranscriptional mechanism: alternative splicing. In comparison to previously reported MACPFs in Arabidopsis, MACP2 shares a redundant but nonoverlapping role in plant immunity. Thus, our findings provide novel insights and genetic tools for the MACPF family in maintaining SA accumulation in response to pathogens in Arabidopsis. [ABSTRACT FROM AUTHOR]

The functions of jasmonic acid (JA) in various stress responses have been uncovered in details, but its role in salt tolerance remains unclear. Here, we characterize the function of Arabidopsis lipoxygenase3 (LOX3), an enzyme involved in JA synthesis, in salt stress response. The transcriptional analysis indicated that LOX3 was dramatically induced under salt treatment. Compared with wild type, the lox3 mutant exhibited hypersensitivity to salt stress in germination and different developmental stages. Interestingly, methyl jasmonate (MeJA) rescued the salt sensitivity phenotypes of the lox3 mutant, suggesting the impairment of salinity response in the mutant may be mediated by JA. Furthermore, the lateral root number of the lox3 mutant was similar with that in wild type under normal condition, but less than that in wild type during salt treatment, and this lateral root sensitivity phenotype was also complemented by exogenous MeJA. In addition, the measurement of oxylipins in the lox3 mutant and the analysis on germination of the JA receptor coi1 mutant under salt stress supported that JA may regulate the early response to salinity. In conclusion, we characterized the novel function of LOX3 in salinity stress response, and found that the salt hypersensitivity of the lox3 mutant can be complemented by MeJA, providing new evidence for the association between JA and salt tolerance. [ABSTRACT FROM AUTHOR]