The OsBZR1-OsGLR3.4 Module Confers Rice Salt Tolerance through the Interplay between Ca2+ and Brassinosteroid Signaling.
TL;DR
A regulatory module OsBZR1-OsGLR3.4-mediated Ca2+ influx regulates rice salt adaptation by interplaying with BR signaling through the interplay between Ca2+ and the BR signaling pathway is revealed.
Abstract
The transient elevation of cytosolic Ca2+ levels is recognized as an essential signal for salt tolerance in plants, whereas the mechanisms for encoding Ca2+ signatures during this process have been largely unknown. Here, we show that glutamate receptor-like channel OsGLR3.4-mediated Ca2+ influx regulates rice salt adaptation by interplaying with BR signaling. Functional loss of OsGLR3.4 leads to decreased salt tolerance coupled with reduced Ca2+ influx, whereas its overexpression markedly enhances salt adaptation in rice. OsBZR1, the key transcription factor in BR signaling, transcriptionally activates OsGLR3.4, which is substantially increased by salt stress. In agreement, the osbzr1 mutant shows decreased salt tolerance with impaired salt-triggered Ca2+ influx, whereas exogenous Ca2+ application rescues its salt-sensitive defects. Genetic evidence showed that OsBZR1 promotes rice salt tolerance, at least partly through OsGLR3.4. Together, this study reveals a regulatory module OsBZR1-OsGLR3.4 that confers rice salt tolerance through the interplay between Ca2+ and the BR signaling pathway.