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

被引:444
作者
Du, Liqun [1 ,2 ]
Ali, Gul S. [4 ,5 ]
Simons, Kayla A. [1 ,2 ]
Hou, Jingguo [3 ]
Yang, Tianbao [1 ,2 ]
Reddy, A. S. N. [4 ,5 ]
Poovaiah, B. W. [1 ,2 ]
机构
[1] Washington State Univ, Ctr Integrated Biotechnol, Pullman, WA 99164 USA
[2] Washington State Univ, Dept Hort, Pullman, WA 99164 USA
[3] Washington State Univ, Dept Chem, Pullman, WA 99164 USA
[4] Colorado State Univ, Dept Biol, Ft Collins, CO 80523 USA
[5] Colorado State Univ, Program Mol Plant Biol, Ft Collins, CO 80523 USA
基金
美国国家科学基金会; 美国农业部;
关键词
SYSTEMIC ACQUIRED-RESISTANCE; CALMODULIN-BINDING PROTEIN; DISEASE-RESISTANCE; TRANSCRIPTIONAL REGULATION; HYPERSENSITIVE RESPONSE; ARABIDOPSIS-THALIANA; SIGNALING PATHWAYS; CELL-DEATH; DEFENSE; FAMILY;
D O I
10.1038/nature07612
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Intracellular calcium transients during plant-pathogen interactions are necessary early events leading to local and systemic acquired resistance(1). Salicylic acid, a critical messenger, is also required for both of these responses(2,3), 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.
引用
收藏
页码:1154 / U116
页数:6
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