%0 Journal Article %1 liu2019anion %A Liu, Y. %A Maierhofer, T. %A Rybak, K. %A Sklenar, J. %A Breakspear, A. %A Johnston, M. G. %A Fliegmann, J. %A Huang, S. %A Roelfsema, M. R. G. %A Felix, G. %A Faulkner, C. %A Menke, F. L. %A Geiger, D. %A Hedrich, R. %A Robatzek, S. %D 2019 %J Elife %K Arabidopsis/drug effects/*immunology myOwn %R 10.7554/eLife.44474 %T Anion channel SLAH3 is a regulatory target of chitin receptor-associated kinase PBL27 in microbial stomatal closure %U https://www.ncbi.nlm.nih.gov/pubmed/31524595 %V 8 %X In plants, antimicrobial immune responses involve the cellular release of anions and are responsible for the closure of stomatal pores. Detection of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) induces currents mediated via slow-type (S-type) anion channels by a yet not understood mechanism. Here, we show that stomatal closure to fungal chitin is conferred by the major PRRs for chitin recognition, LYK5 and CERK1, the receptor-like cytoplasmic kinase PBL27, and the SLAH3 anion channel. PBL27 has the capacity to phosphorylate SLAH3, of which S127 and S189 are required to activate SLAH3. Full activation of the channel entails CERK1, depending on PBL27. Importantly, both S127 and S189 residues of SLAH3 are required for chitin-induced stomatal closure and anti-fungal immunity at the whole leaf level. Our results demonstrate a short signal transduction module from MAMP recognition to anion channel activation, and independent of ABA-induced SLAH3 activation.

@article{liu2019anion, abstract = {In plants, antimicrobial immune responses involve the cellular release of anions and are responsible for the closure of stomatal pores. Detection of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) induces currents mediated via slow-type (S-type) anion channels by a yet not understood mechanism. Here, we show that stomatal closure to fungal chitin is conferred by the major PRRs for chitin recognition, LYK5 and CERK1, the receptor-like cytoplasmic kinase PBL27, and the SLAH3 anion channel. PBL27 has the capacity to phosphorylate SLAH3, of which S127 and S189 are required to activate SLAH3. Full activation of the channel entails CERK1, depending on PBL27. Importantly, both S127 and S189 residues of SLAH3 are required for chitin-induced stomatal closure and anti-fungal immunity at the whole leaf level. Our results demonstrate a short signal transduction module from MAMP recognition to anion channel activation, and independent of ABA-induced SLAH3 activation.}, added-at = {2024-02-15T15:08:22.000+0100}, author = {Liu, Y. and Maierhofer, T. and Rybak, K. and Sklenar, J. and Breakspear, A. and Johnston, M. G. and Fliegmann, J. and Huang, S. and Roelfsema, M. R. G. and Felix, G. and Faulkner, C. and Menke, F. L. and Geiger, D. and Hedrich, R. and Robatzek, S.}, biburl = {https://www.bibsonomy.org/bibtex/2084baafad23d8f51ac87bca400c7ac9c/jvsi_all}, doi = {10.7554/eLife.44474}, interhash = {1d5f91f11e32f444421c6ce86408ba04}, intrahash = {084baafad23d8f51ac87bca400c7ac9c}, issn = {2050-084X (Electronic) 2050-084X (Linking)}, journal = {Elife}, keywords = {Arabidopsis/drug effects/*immunology myOwn}, note = {Liu, Yi Maierhofer, Tobias Rybak, Katarzyna Sklenar, Jan Breakspear, Andy Johnston, Matthew G Fliegmann, Judith Huang, Shouguang Roelfsema, M Rob G Felix, Georg Faulkner, Christine Menke, Frank Lh Geiger, Dietmar Hedrich, Rainer Robatzek, Silke eng Group Leader Fellowship/Gatsby Charitable Foundation/International Project Award/H2020 European Research Council/International Project Award/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom Project Award/Deutsche Forschungsgemeinschaft/International Heisenberg Fellowship/Deutsche Forschungsgemeinschaft/International Research Support, Non-U.S. Gov't England 2019/09/17 Elife. 2019 Sep 16;8:e44474. doi: 10.7554/eLife.44474.}, timestamp = {2024-02-15T15:08:22.000+0100}, title = {Anion channel SLAH3 is a regulatory target of chitin receptor-associated kinase PBL27 in microbial stomatal closure}, type = {Journal Article}, url = {https://www.ncbi.nlm.nih.gov/pubmed/31524595}, volume = 8, year = 2019 }