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Knowing your friends and foes – plant receptor‐like kinases as initiators of symbiosis or defence
Author(s) -
AntolínLlovera Meritxell,
Petutsching Elena Kristin,
Ried Martina Katharina,
Lipka Volker,
Nürnberger Thorsten,
Robatzek Silke,
Parniske Martin
Publication year - 2014
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.13117
Subject(s) - ectodomain , biology , microbiology and biotechnology , kinase , internalization , symbiosis , receptor , signalling , endocytosis , protein kinase domain , signal transduction , phosphorylation , biochemistry , genetics , bacteria , mutant , gene
Summary The decision between defence and symbiosis signalling in plants involves alternative and modular plasma membrane‐localized receptor complexes. A critical step in their activation is ligand‐induced homo‐ or hetero‐oligomerization of leucine‐rich repeat ( LRR )‐ and/or lysin motif (LysM) receptor‐like kinases ( RLK s). In defence signalling, receptor complexes form upon binding of pathogen‐associated molecular patterns ( PAMP s), including the bacterial flagellin‐derived peptide flg22, or chitin. Similar mechanisms are likely to operate during the perception of microbial symbiont‐derived (lipo)‐chitooligosaccharides. The structurally related chitin‐oligomer ligands chitooctaose and chitotetraose trigger defence and symbiosis signalling, respectively, and their discrimination involves closely related, if not identical, LysM‐ RLK s. This illustrates the demand for and the challenges imposed on decision mechanisms that ensure appropriate signal initiation. Appropriate signalling critically depends on abundance and localization of RLK s at the cell surface. This is regulated by internalization, which also provides a mechanism for the removal of activated signalling RLK s. Abundance of the malectin‐like domain ( MLD )‐ LRR ‐ RLK Symbiosis Receptor‐like Kinase ( SYMRK ) is additionally controlled by cleavage of its modular ectodomain, which generates a truncated and rapidly degraded RLK fragment. This review explores LRR ‐ and LysM‐mediated signalling, the involvement of MLD ‐ LRR ‐ RLK s in symbiosis and defence, and the role of endocytosis in RLK function.