Fig. 1

PRRs and NLRs involved in Phytophthora resistance. Cell surface pattern recognition receptors (PRRs) (ELR, EIR1, RE02, RXEG1, REL, ERK1, RLP23, and RDA2) interact with SOBIR1 and BAK1 to form PRR immune complexes upon recognition of pathogen-associated molecular pattern (PAMPs) or apoplastic effectors from Phytophthora pathogens. Activation of PRRs triggers phosphorylation of receptor-like cytoplasmic kinases (RLCKs), RBOHD, PIPs, and Ca²⁺ channels, leads to production of reactive oxygen species (ROS), influx of calcium, the MAP kinase cascade activation and downstream defense-related gene expression. Other RLKs (LecRK-IX.2, LecRK-I.9, LecRK-IX.1, LecRK-IV.4, LecRK-V.5, and GmLMM1) play positive roles in resistance to Phytophthora pathogens as well. Pathogens also deliver race-specific effector proteins to suppress host immunity in various modes to facilitate infection. In this context, cytoplasmic nucleotide-binding leucine-rich repeat (NLR) receptors (NLRs), including CC-NBD-LRR (CNL) proteins and TIR-NBD-LRR (TNL) proteins, sense a portion of these effectors and activate another layer of plant immunity known as effector-triggered immunity (ETI). In such cases, recognized effectors are referred to as avirulence (Avr) proteins. ETI also leads to a number of overlapping downstream outputs consistent with pattern-triggered immunity (PTI), and usually with stronger amplitudes compared to PTI