Anion channel SLAH3 is a regulatory target of chitin receptor-associated kinase PBL27 in microbial stomatal closure
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.
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All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided for main and supplemental figures.
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Author details
Funding
Gatsby Charitable Foundation (Group Leader Fellowship)
- Silke Robatzek
H2020 European Research Council (Project Award)
- Silke Robatzek
Biotechnology and Biological Sciences Research Council (Project Award)
- Christine Faulkner
Deutsche Forschungsgemeinschaft (Project Award)
- Dietmar Geiger
- Rainer Hedrich
Deutsche Forschungsgemeinschaft (Project Award)
- Rainer Hedrich
Deutsche Forschungsgemeinschaft (Heisenberg Fellowship)
- Silke Robatzek
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2019, Liu et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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