title: The roles of anion channels in Arabidopsis immunity.
abstract: Anion efflux is one of the most immediate responses of plant cells to pathogen attacks, suggesting that anion channels may play a role in plant defense. Recently we reported that the chloride channel AtCLCd negatively regulates Arabidopsis pathogen-associated molecular pattern-triggered immunity (PTI), probably by affecting trafficking of the pattern recognition receptors (PRRs). Since AtCLCd is localized to the trans-Golgi network, it is not likely to be directly involved in anion flux across the plasma membrane. Here, we used a pharmacological approach to explore further the function of plasma membrane-localized R-type and S-type anion channels in plant immunity. We found that the R-type and S-type anion channels play opposite roles in Arabidopsis innate immunity. Inhibition of the R-type anion channels enhances, whereas inhibition of the S-type channels inhibits PTI and effector-triggered immunity (ETI).
authors.affiliation: a State Key Laboratory of Plant Genomics; Institute of Microbiology; Chinese Academy of Sciences; Beijing, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Guo
authors.forename: Chengcheng
authors.initials: C
authors.lastname: Wang
authors.forename: Zhangli
authors.initials: Z
authors.lastname: Zuo
authors.forename: Jin-Long
authors.initials: JL
authors.lastname: Qiu
mesh_terms: D000838:Anions / Q000378:metabolism*; D017360:Arabidopsis / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism; D060467:Disease Resistance; D007473:Ion Channels / Q000378:metabolism*; D010935:Plant Diseases; D021381:Protein Transport; D051192:Receptors, Pattern Recognition / Q000378:metabolism; D021601:trans-Golgi Network
chemical_list: D000838:Anions; D029681:Arabidopsis Proteins; D002712:Chlorides; D007473:Ion Channels; D051192:Receptors, Pattern Recognition
keywords: Arabidopsis; PAMP-triggered immunity; anion channel; effector-triggered immunity