Intracellular calcium changes during plant–pathogen interaction are essential early events leading to both local and systemic acquired resistances. Salicylic acid, a critical messenger, is also required for both responses. However, the relationship between the CBL-CIPK and SA signaling pathways during wheat–Pst interaction is unclear. In this study, we isolated seven wheat CBL and 11 wheat CIPK genes and designated them as TaCBL1, 2, 3, 4, 6, 7, 9 and TaCIPK2, 5, 7, 9, 10, 14, 15, 17, 23, 31, 32. Some wheat CBLs and CIPKs were functionally characterized. Concurrently, wheat TaNPR1 as a master regulator of SA-mediated host response during Pst infection was functionally characterized. Silencing of TaCBL4, TaCIPK10 and TaNPR1 permitted increased rust development in a wheat variety that was resistant to Pst pathotype CYR23. Decreased levels of salicylic acid (SA) were observed in TaCBL4- and TaCIPK10-silenced wheat plants. Yeast two-hybrid and biomolecular fluorescence complementation (BiFC) revealed that TaCIPK10 interacted with both TaCBL4 and TaNPR1. These results suggest that a TaCBL4-TaCIPK10-TaNPR1 complex is involved in innate immunity of wheat to Pst.
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