Nature 457, 1154-1158 (26 February 2009) | doi:10.1038/nature07612; Received 9 August 2008; Accepted 4 November 2008; Published online 4 January 2009

Ca2+/calmodulin regulates salicylic-acid-mediated plant immunity

Liqun Du1, Gul S. Ali3, Kayla A. Simons1, Jingguo Hou2,4, Tianbao Yang1, A. S. N. Reddy3 & B. W. Poovaiah1

  1. Center for Integrated Biotechnology and Department of Horticulture,
  2. Department of Chemistry, Washington State University, Pullman, Washington 99164-6414, USA
  3. Department of Biology and Program in Molecular Plant Biology, Colorado State University, Fort Collins, Colorado 80523-1878, USA
  4. Present address: Bioanalytical Services, Primera Analytical Solutions Corp., 259 Wall Street, Princeton, New Jersey 08540, USA.

Correspondence to: B. W. Poovaiah1 Correspondence and requests for materials should be addressed to B.W.P. (Email: poovaiah@wsu.edu).

Intracellular calcium transients during plant–pathogen interactions are necessary early events leading to local and systemic acquired resistance1. Salicylic acid, a critical messenger, is also required for both of these responses2, 3, but whether and how salicylic acid level is regulated by Ca2+ signalling during plant–pathogen interaction is unclear. Here we report a mechanism connecting Ca2+ signal to salicylic-acid-mediated immune response through calmodulin, AtSR1 (also known as CAMTA3), a Ca2+/calmodulin-binding transcription factor, and EDS1, an established regulator of salicylic acid level. Constitutive disease resistance and elevated levels of salicylic acid in loss-of-function alleles of Arabidopsis AtSR1 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. We show that AtSR1 interacts with the promoter of EDS1 and represses its expression. Furthermore, Ca2+/calmodulin-binding to AtSR1 is required for suppression of plant defence, indicating a direct role for Ca2+/calmodulin in regulating the function of AtSR1. These results reveal a previously unknown regulatory mechanism linking Ca2+ signalling to salicylic acid level.


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