Fig. 3

Diagram of pattern-triggered immunity (PTI) signalling in response to PAMPs and effector-triggered immunity (ETI) signalling in response to plant effectors. During various pathogen infections, many PAMPs/DAMPs are recognized by plasma membrane-localized RLP complexes. The LRR-RLPs NbREli and LysM-RLPs OsCEBiP recognize PpEli2 and chitin, respectively. REli recognizes PpEli2 and forms a complex with two co-receptors, BAK1 and SOBIR1, to trigger the downstream immune responses, including HR cell death and ROS burst. Chitin is sensed by OsCEBiP. Activated OsCEBiP binds to the co-receptor OsCERK1 to form the OsCEBiP-OsCERK1 complex that initiates OsRacGEF1-dependent chitin signalling pathways. The OsCEBiP-OsCERK1 complex mediates the phosphorylation of OsRacGEF1 (a guanine nucleotide exchange factor for OsRac1), activating the small GTPase OsRac1. Subsequently, the OsRAI1 transcription factor is activated, further upregulating the expression of defense-related genes, leading to disease resistance. OsRLCK185 is essential for chitin-triggered immune responses. In N. benthamiana, Cf-4 requires the intracellular nucleotide-binding domain leucine-rich repeat-containing receptor (NLR) NRC3 to trigger a confluent cell death response upon detecting the fungal effector Avr4. Following the perception of Avr4 by Cf-4, the kinase domains of SOBIR1 and BAK1 directly phosphorylate each other. Avr4/Cf-4 can trigger ROS accumulation and MAPK activation in RLCK-VII-6, -7, and − 8-dependent manner, whereas members of RLCK-VII-7 are also required for the Avr4/Cf-4-induced HR