Pattern-recognition receptors are required for NLR-mediated plant immunity

The plant immune system is fundamental to the survival and productivity of plants in crop fields and natural ecosystems. Substantial evidence supports the prevailing notion that plants have evolved two branches of innate immune signaling, called pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is triggered by conserved microbial patterns via surface-localized pattern-recognition receptors (PRRs), whereas ETI is activated by pathogen effector proteins via mostly intracellularly-localized receptors called nucleotide-binding, leucine-rich repeat proteins (NLRs). PTI and ETI have traditionally been considered to be separate immune signaling pathways and have evolved sequentially. Here we show that, contrary to the perception of PTI and ETI being separate immune signaling pathways, Arabidopsis PRR/co-receptor mutants, fls2/efr/cerk1 and bak1/bkk1/cerk1 triple mutants, are greatly compromised in ETI responses triggered by Pseudomonas syrinage effectors. We further identified the NADPH oxidase (RBOHD)-mediated production of reactive oxygen species as a critical early signaling event connecting PRR and NLR signaling cascades and show that PRR-mediated activation of RBOHD is necessary for full activation of RBOHD during ETI. Furthermore, NLR signaling rapidly augments the transcript and protein levels of key PTI components at an early stage and in a salicylic acid-independent manner. Our study supports an alternative model in which PTI is in fact an indispensable component of ETI during bacterial infection, implying that ETI halts pathogen infection, in part, by directly co-opting the anti-pathogen mechanisms proposed for PTI. This alternative model conceptually unites two major immune signaling pathways in the plant kingdom and mechanistically explains the long-observed similarities in downstream defense outputs between PTI and ETI.