Faculty of Biology, Genetics, University of Munich (LMU), 82152, Martinsried, Germany.
New Phytol. 2014 Dec;204(4):791-802. doi: 10.1111/nph.13117.
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 (RLKs). In defence signalling, receptor complexes form upon binding of pathogen-associated molecular patterns (PAMPs), 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-RLKs. 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 RLKs at the cell surface. This is regulated by internalization, which also provides a mechanism for the removal of activated signalling RLKs. 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-RLKs in symbiosis and defence, and the role of endocytosis in RLK function.
在植物中,防御和共生信号之间的选择涉及替代和模块化的质膜定位受体复合物。它们激活的关键步骤是富含亮氨酸重复(LRR)和/或赖氨酰基(LysM)基序受体样激酶(RLK)的配体诱导同型或异型寡聚化。在防御信号转导中,受体复合物在结合病原体相关分子模式(PAMPs)时形成,包括细菌鞭毛衍生肽 flg22 或几丁质。在感知微生物共生衍生(脂)-几丁寡糖时,可能会发生类似的机制。结构相关的几丁寡糖配体壳寡糖八糖和壳四糖分别触发防御和共生信号转导,其识别涉及密切相关的,如果不是相同的,LysM-RLKs。这说明了确保适当信号起始的决策机制的需求和挑战。适当的信号转导严重依赖于 RLK 在细胞表面的丰度和定位。这是通过内化来调节的,内化也提供了一种去除激活的信号转导 RLK 的机制。类糜蛋白酶样结构域(MLD)-LRR-RLK 共生受体样激酶(SYMRK)的丰度还受其模块化胞外结构域切割的控制,这会产生一个截短的、迅速降解的 RLK 片段。这篇综述探讨了 LRR 和 LysM 介导的信号转导、MLD-LRR-RLK 在共生和防御中的参与以及内吞作用在 RLK 功能中的作用。