Rice OsBBX17 encodes a B-box zinc finger transcription factor in which the N-terminal B-box structural domain interacts with OsMPK1. In addition, it directly binds to the G-box of OsHAK2 and OsHAK7 promoters and represses their transcription. Under saline-alkaline conditions, the expression of OsBBX17 was inhibited. Meanwhile, activation of the OsMPK1-mediated mitogen-activated protein kinase cascade pathway caused OsMPK1 to interact with OsBBX17 and phosphorylate OsBBX17 at the Thr-95 site. It reduced OsBBX17 DNA-binding activity and enhanced saline-alkaline tolerance by deregulating transcriptional repression of OsHAK2 and OsHAK7. Genetic assays showed that the osbbx17-KO had an excellent saline-alkaline tolerance, whereas the opposite was in OsBBX17-OE. In addition, overexpression of OsMPK1 significantly improved saline-alkaline tolerance, but knockout of OsMPK1 caused an increased sensitivity. Further overexpression of OsBBX17 in the osmpk1-KO caused extreme saline-alkaline sensitivity, even a quick death. OsBBX17 was validated in saline-alkaline tolerance from two independent aspects, transcriptional level and post-translational protein modification, unveiling a mechanistic framework by which OsMPK1-mediated phosphorylation of OsBBX17 regulates the transcription of OsHAK2 and OsHAK7 to enhance the Na+ /K+ homeostasis, which partially explains light on the molecular mechanisms of rice responds to saline-alkaline stress via B-box transcription factors for the genetic engineering of saline-alkaline tolerant crops.
Keywords: MAPK cascade pathway; Na+/K+ homeostasis; protein phosphorylation; rice; saline-alkaline stress; transcriptional regulation.
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