Guo Wei, Zuo Zhangli, Cheng Xi, Sun Juan, Li Huali, Li Legong, Qiu Jin-Long
State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
J Exp Bot. 2014 Mar;65(4):1205-15. doi: 10.1093/jxb/ert484. Epub 2014 Jan 21.
Chloride channel (CLC) family genes are ubiquitous from prokaryotes to eukaryotes and encode proteins with both channel and transporter activities. The Arabidopsis thaliana genome encodes seven CLC genes, and their products are found in a variety of cellular compartments and have various physiological functions. However, a role for AtCLCs in plant innate immunity has not previously been demonstrated. Here it is reported that AtCLCd is a negative regulator of pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). T-DNA insertion mutants of AtCLCd exhibited enhanced responses to the elicitor, flg22. The PTI phenotypes of the clcd mutants were rescued by expression of AtCLCd. Overexpression of AtCLCd led to impaired flg22-induced responses. In line with a role for AtCLCd in PTI, the clcd mutants were more resistant to a virulent strain of the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 when spray inoculated, while AtCLCd-overexpressing lines displayed increased susceptibility to this pathogen. Interestingly, flg22 treatment was found to repress the expression of AtCLCd. In addition, its expression was elevated in mutants of the flg22 pattern recognition receptor (PRR) FLS2 and the PRR regulatory proteins BAK1 and BKK1, and reduced in an FLS2-overexpressing line. These latter findings indicate that FLS2 complexes regulate the expression of AtCLCd, further supporting a role for AtCLCd in PTI.
氯离子通道（CLC）家族基因在从原核生物到真核生物中普遍存在，编码具有通道和转运蛋白活性的蛋白质。拟南芥基因组编码七个CLC基因，其产物存在于多种细胞区室中并具有多种生理功能。然而，AtCLCs在植物先天免疫中的作用此前尚未得到证实。本文报道AtCLCd是病原体相关分子模式（PAMP）触发的免疫（PTI）的负调控因子。AtCLCd的T-DNA插入突变体对激发子flg22表现出增强的反应。AtCLCd的表达挽救了clcd突变体的PTI表型。AtCLCd的过表达导致flg22诱导的反应受损。与AtCLCd在PTI中的作用一致，clcd突变体在喷雾接种时对细菌病原体番茄丁香假单胞菌pv. tomato DC3000的强毒株更具抗性，而AtCLCd过表达系对该病原体的敏感性增加。有趣的是，发现flg22处理会抑制AtCLCd的表达。此外，其在flg22模式识别受体（PRR）FLS2以及PRR调节蛋白BAK1和BKK1的突变体中表达升高，而在FLS2过表达系中表达降低。后一发现表明FLS2复合物调节AtCLCd的表达，进一步支持AtCLCd在PTI中的作用。
