A B‐box transcription factor OsBBX17 regulates saline‐alkaline tolerance through the MAPK cascade pathway in rice

Abstract

Summary 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.