Abstract
Background: Sensing and responding to stresses determine the tolerance of plants to adverse environments. The triploid Chinese white poplar is widely cultivated in North China because of its adaptation to a wide range of habitats including highly saline ones. However, its triploid genome complicates any detailed investigation of the molecular mechanisms underlying its adaptations. Results: We report a haplotype-resolved genome of this triploid poplar and characterize, using reverse genetics and biochemical approaches, a MYB gene, SALT RESPONSIVE MYB TRANSCRIPTION FACTOR (SRMT), which combines NUCLEAR FACTOR Y SUBUNIT C 9 (PtoNF-YC9) and RESPONSIVE TO DESICCATION 26 (PtoRD26), to regulate an ABA-dependent salt-stress response signaling. We reveal that the salt-inducible PtoRD26 is dependent on ABA signaling. We demonstrate that ABA or salt drives PtoNF-YC9 shuttling into the nucleus where it interacts with SRMT, resulting in the rapid expression of PtoRD26 which in turn directly regulates SRMT. This positive feedback loop of SRMT-PtoRD26 can rapidly amplify salt-stress signaling. Interference with either component of this regulatory module reduces the salt tolerance of this triploid poplar. Conclusion: Our findings reveal a novel ABA-dependent salt-responsive mechanism, which is mediated by the PtoNF-YC9-SRMT-PtoRD26 module that confers salt tolerance to this triploid poplar. These genes may therefore also serve as potential and important modification targets in breeding programs.