Phytochrome B-mediated light signalling enhances rice resistance to saline-alkaline and sheath blight by regulating multiple downstream transcription factors

Abstract

Light signalling regulates plant growth and stress resistance, whereas its mechanism in controlling saline-alkaline tolerance (SAT) remains largely unknown. This study identified that light signalling, primarily mediated by Phytochrome B (PhyB), inhibited ammonium transporter 1 (AMT1) to negatively regulate SAT. Our previous findings have shown that PhyB can impede the transcription factors indeterminate domain 10 (IDD10) and brassinazole resistant 1 (BZR1) to reduce NH4+ uptake, thereby modulating SAT and sheath blight (ShB) resistance in rice. However, inhibition of IDD10 and BZR1 in the phyB background did not fully suppress NH4+ uptake, suggesting that other signalling pathways regulated AMT1 downstream of PhyB. Further analysis revealed that PhyB interacted with Calcineurin B-like protein-interacting protein kinase 31 (CIPK31), which positively regulated AMT1 expression. CIPK31 also interacted with Teosinte Branched1/Cycloidea/PCF19 (TCP19), a key regulator of nitrogen use efficiency (NUE). However, PhyB neither degraded CIPK31 nor directly interacted with TCP19. Instead, PhyB inhibited the CIPK31-TCP19 interaction, releasing TCP19, which repressed AMT1;2 directly and AMT1;1 and AMT1;3 indirectly, thereby inhibiting NH4+ uptake and SAT while reducing ShB resistance. Additionally, Phytochrome Interacting Factor-Like 15 (PIL15) interacted with TCP19. Different from TCP19, PIL15 directly activated AMT1;2 to promote SAT, suggesting a balancing mechanism for NH4+ uptake downstream of PhyB. Furthermore, PIL15 interacted with IDD10 and BZR1 to form a transcriptional complex that collaboratively activated AMT1;2 expression. Overall, this study provides novel insights into how PhyB signalling regulates NH4+ uptake and coordinates SAT and ShB resistance in rice.