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WRKY transcription factors play a role in a variety of biological processes. Several studies have revealed that abiotic stress regulates the transcription of a large number of WRKY genes. In this study, we report the identification of a novel ' SAPK10 - WRKY87 - ABF1 ' biological pathway, through which they harmoniously enhance drought and salinity tolerance. We generated OsWRKY87 -overexpressing transgenic rice and found that the transgenic seedlings exhibited significantly improved drought and salinity stress tolerance. Subcellular localization in rice seedling protoplast revealed that OsWRKY87-GFP fusion protein mostly accumulated in the nucleus, suggesting that OsWRKY87 is a nucleus-localized protein, in line with the predicted function of OsWRKY87 as a transcription factor. In vivo interaction between SAPK10 and WRKY87 was demonstrated by Yeast two-hybrid-assay. In addition, phosphorylation assays showed that SAPK10 exhibits autophosphorylation activity on the 177th serine, enabling it to phosphorylate WRKY87. OsWRKY87 functioned as a transcriptional initiator, according to a yeast one-hybrid assay and a luciferase assay. Remarkably, gel mobility shift assay showed that phosphorylated WRKY87 enhances its DNA-binding ability to the W-box cis-element of ABF1 promoter and activated its transcription, thereby elevating the ABF1 transcription and improving drought and salinity tolerance. Overall, our findings revealed a novel ' SAPK10- WRKY87-ABF1 ' module, which synergistically interacts to improve drought and salt tolerance in rice (Oryza sativa). • A novel SAPK10 - WRKY87 - ABF1 pathway, enhance drought and salt tolerance in rice. • OsWRKY87-GFP fusion protein accumulated mainly in the nucleus • SAPK10 exhibits autophosphorylation, enabling it to phosphorylate WRKY87 • EMSA revealed that phosphorylated WRKY87 enhances its DNA-binding ability • OXWRKY87 plants exhibited enhanced tolerance to drought and salt stresses [ABSTRACT FROM AUTHOR]

Vibrio harveyi is a zoonotic pathogen that can infect humans through wounds and cause severe inflammatory responses. Previous studies have reported that the Toll like receptors (TLR) mediated MAPK, AKT and NF-κB signaling pathways are involved in innate immune system resistance to pathogen invasion. However, the molecular mechanism of these pathways, as well as their involvement in V. harveyi infection remains elusive. This study established a V. harveyi infection model using murine peritoneal macrophages (PMs). Various techniques, including western blotting, ELISA, RT-qPCR, immunofluorescence, inhibition assays, were used to explore the roles of TLRs, MAPK, AKT and NF-κB signaling pathways in V. harveyi -induced inflammatory responses. ELISA assays showed that V. harveyi infection triggered proinflammatory cytokines secretion in PMs. RT-qPCR and inhibition assays showed that TLR2 participated in V. harveyi infection and up-regulated the proinflammatory cytokines secretion in murine PMs. Western blotting data showed that the phosphorylation of p38, JNK, AKT, and NF-κB p65 were significantly increased partly mediated by TLR2. In addition, immunofluorescence assays revealed that the NF-κB p65 translocated into nucleus in response to V. harveyi infection. The secretion of IL-1β, IL-6, IL-12, and TNF-α were considerably reduced when the p38 MAPK and NF-κB signaling pathways were blocked, whereas blocking of AKT significantly increased the expression of IL-1β, IL-6, IL-12, and TNF-α. These findings indicate that V. harveyi infection induces inflammatory responses in murine PMs via activation of p38 MAPK and NF-κB pathways, which are partly mediated by TLR2, but are inhibited by PI3K/AKT pathways. • V. harveyi induces inflammatory responses in murine PMs. • The MAPK, AKT and NF-κB pathways were activated against V. harveyi infection in PMs. • V. harveyi induce inflammation in PMs via p38 MAPK and NF-κB pathways. • Activation of AKT pathway relieve V. harveyi induced inflammatory responses in PMs. [ABSTRACT FROM AUTHOR]