Receptor-like cytoplasmic kinases (RLCKs) play crucial roles in regulating plant development and immunity. Conserved pathogen-associated molecular patterns (PAMPs) derived from microbes are recognized by plant pattern recognition receptors to activate PAMP-triggered immunity (PTI). Microbial effectors, whose initial function is to promote virulence, are recognized by plant intracellular nucleotide-binding domain and leucine-rich repeat receptors (NLRs) to initiate effector-triggered immunity (ETI). Both PTI and ETI trigger early immune signaling events including the production of reactive oxygen species, induction of calcium influx and activation of mitogen-activated protein kinases. Research progress has revealed the important roles of RLCKs in the regulation of early PTI signaling. Accordingly, RLCKs are often targeted by microbial effectors that are evolved to evade PTI via diverse modulations. In some cases, modulation of RLCKs by microbial effectors triggers the activation of NLRs. This review covers the mechanisms by which RLCKs engage diverse substrates to regulate early PTI signaling and the regulatory roles of RLCKs in triggering NLR activation. Accumulating evidence suggests evolutionary links and close connections between PAMP- and effector-triggered early immune signaling that are mediated by RLCKs. As key immune regulators, RLCKs can be considered targets with broad prospects for the improvement of plant resistance via genetic engineering.
Keywords: NLR; PAMP-triggered immunity; PRR; effector-triggered immunity; phosphorylation; receptor-like cytoplasmic kinase.
© FEMS 2020.