Fig 1.
Schematic models for synergies between cell-surface and intracellular receptor-mediated signaling.
(A) Upon ligand perception, PRRs recruit coreceptors (e.g., BAK1, CERK1) to phosphorylate each other and the downstream RLCKs. The activated RLCKs further induce Ca2+ influx by phosphorylating Ca2+ channels. Studies show that PTI up-regulates the transcription of TNL or TIR domain-containing genes, which requires PRR-initiated calcium flux. The cell-surface localized coreceptor SOBIR1 interacts with EDS1-helper NLR complexes to form supramolecular complexes in a ligand-independent manner, to potentially regulate PTI. Some RLCK proteins (e.g., PBL19) are cleaved by metacaspases like MC4 to generate truncated RLCKs, which phosphorylate EDS1 in the cytoplasm to boost plant resistance. (B) Activated TNL resistosomes serve as NAD+-cleaving enzymes and 2′,3′-cAMP/cGMP synthetase. NAD+-derived small molecules are produced and activate EDS1-helper NLR complexes. CNL and helper NLR (or RNL) resistosomes form calcium-permeable channels triggering immune signaling. A recent study suggests that the formation of RNL resistosome requires both PRR and TNL signaling. Similarly, activation of RBOHD-mediating ROS burst relies on both PRR and NLR signaling. Activation of MAPK cascades by TNLs requires PRR signaling. ETI increases the transcript and protein levels of many key components of PRR pathway, possibly through members of CBP60 transcription factor family. Black arrows indicate the regulation by cell-surface receptor pathway, and red arrows indicate the regulation by intracellular receptor pathway. Solid arrows indicate direct effects, and dashed ones indicate indirect effects where the mechanism is unclear. Created with BioRender.com. CNL, coiled-coil-type NLR; ETI, effector-triggered immunity; MAPK, mitogen-activated protein kinase; NLR, nucleotide-binding domain leucine-rich repeat receptor; PAMP, pathogen-associated molecular pattern; PPR, pattern recognition receptor; PTI, pattern-triggered immunity; RLCK, receptor-like cytoplasmic kinase; RNL, Resistance to powdery mildew 8-like domain (RPW8)-type NLR; ROS, reactive oxygen species; TIR, Toll/interleukin-1 receptor/Resistance protein; TNL, TIR-type NLR.
Fig 2.
Conservation of synergies between cell-surface and intracellular receptor-mediated signaling in different plant pathosystems.
Studies suggest a similar mode of synergistic interactions between cell surface and intracellular receptor pathways in some other plant species, but different forms of interplay between the two pathways may also exist. More studies are needed in the future to get a clear and full picture of plant immune networks in diverse species. Created with BioRender.com.