植物细胞能够探知病原体，从而激发一个让植物对感染产生抵抗力的防卫系统。植物防卫通道中一个最早的步骤涉及胞质溶解钙水平的增加。然而，Ca2+信号导致有效植物免疫响应的机制尚不清楚。
水杨酸是局部及系统抵抗力的一个关键信使。在这项研究中，Du等人报告了Ca2+信号作用与由水杨酸调节的响应之间的一个新颖联系。他们发现，AtSR1/CAMTA3（一个Ca2+/钙调蛋白—结合转录因子）通过抑制EDS1（水杨酸的一个关键调控因子）抑制水杨酸的响应。突变的AtSR1导致水杨酸水平增加和对丁香假单胞菌等病原体的抵抗力增强。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 457, 1154-1158 (26 February 2009) | doi:10.1038/nature07612
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.
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.
