植物細(xì)胞能夠探知病原體，從而激發(fā)一個(gè)讓植物對(duì)感染產(chǎn)生抵抗力的防衛(wèi)系統(tǒng),。植物防衛(wèi)通道中一個(gè)最早的步驟涉及胞質(zhì)溶解鈣水平的增加,。然而,，Ca2+信號(hào)導(dǎo)致有效植物免疫響應(yīng)的機(jī)制尚不清楚,。
水楊酸是局部及系統(tǒng)抵抗力的一個(gè)關(guān)鍵信使。在這項(xiàng)研究中，Du等人報(bào)告了Ca2+信號(hào)作用與由水楊酸調(diào)節(jié)的響應(yīng)之間的一個(gè)新穎聯(lián)系,。他們發(fā)現(xiàn),，AtSR1/CAMTA3（一個(gè)Ca2+/鈣調(diào)蛋白—結(jié)合轉(zhuǎn)錄因子）通過抑制EDS1（水楊酸的一個(gè)關(guān)鍵調(diào)控因子）抑制水楊酸的響應(yīng)。突變的AtSR1導(dǎo)致水楊酸水平增加和對(duì)丁香假單胞菌等病原體的抵抗力增強(qiáng),。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
