Unmet Need: Understanding the mechanism of regulation of salicylic acid by Ca2+ signaling
Intracellular calcium transients during plant-pathogen interactions are necessary early events leading to local and systemic acquired resistance. Salicylic acid, a critical messenger, is also required for both these responses, but whether and how salicylic acid level is regulated by Ca2+ signaling during plant-pathogen interaction is unclear.
The Technology: Study of novel of regulatory mechanism linking Ca2+ signaling to Salicylic acid level.
Here a novel mechanism connecting Ca2+ signal to salicylic acid-mediated immune response through calmodulin, AtSR1/CAMTA3, a Ca2+/calmodulin-binding transcription factor, and EDS1, an established regulator of salicylic acid level, is reported. Constitutive disease resistance and elevated levels of salicylic acid in loss-of-function alleles of AtSR1/CAMTA3 suggest that AtSR1 is a negative regulator of plant immunity. This was confirmed by epistasis analysis with mutants of compromised salicylic acid accumulation and disease resistance. This WSU research shows that AtSR1 interacts with the promoter of EDS1 and represses its expression. Furthermore, Ca2+/calmodulin-binding to AtSR1 is required for suppression of plant defense, indicating a direct role for Ca2+/calmodulin in regulating the function of AtSR1. These results revealed a novel regulatory mechanism linking Ca2+ signaling to salicylic acid level.
• Agriculture industry
• A novel regulatory mechanism linking Ca2+ signaling to salicylic acid level.
US Patent application filed(US-2010-0223690-A1):