Gibberellic acid signaling promotes resistance to saline–alkaline stress by increasing the uptake of ammonium in rice

Abstract Gibberellic acid (GA) plays important roles in diverse biological processes in plants. However, its function in the resistance of rice ( Oryza sativa ) to saline-alkaline (SAK) stress is unclear. In this study, we found that SAK stimuli changed the levels of expression of the GA signaling genes. Genetic analyses using the mutants of key GA signaling regulators Slender rice 1 (SLR1) and Dwarf 1(D1) demonstrated that SLR1 negatively regulated the resistance of rice to SAK stress, while D1 positively regulated it, suggesting the GA signaling positively regulates the resistance of rice to SAK. A previous study showed that SLR1 interacts with Phytochrome interacting factor-like 14 (PIL14) to regulate the resistance of rice to salt stress. However, PIL14 overexpressor ( OX ) plants exhibited a similar response to SAK as the wild-type (WT) controls. Further analyses revealed that SLR1 interacted with and inhibited the activation of transcription of IDD10 and bZIP23. Furthermore, IDD10 interacted with bZIP23 to activate Ammonium transporter 1;2 ( AMT1;2 ), and slr1 , IDD10 OX and bZIP23 OX accumulated more ammonium (NH 4 + ) than the WT plants. In addition, the bzip23 T-DNA mutant was more sensitive to SAK, while bZIP23 OX was less sensitive compared with the WT. This suggested that bZIP23 is similar to IDD10, which positively regulates the resistance of rice to SAK. Taken together, this data proved that GA signaling promotes the resistance of rice to SAK by modulating the uptake of NH 4 + in rice mediated by SLR1-IDD10-bZIP23.