Abstract
Plants perceive pathogen-associated molecular patterns (PAMPs) using plasma-membrane-localized pattern recognition receptors (PRRs) to activate broad-spectrum pattern-triggered immunity. However, the regulatory mechanisms that ensure robust broad-spectrum plant immunity remain largely unknown. Here, we reveal that the transcription factor WRKY8 has a dual role in the transcriptional regulation of PRR genes: repressing expression of the nlp20/nlp24 receptor gene RLP23 while promoting that of the chitin receptor gene CERK1. SsNLP1 and SsNLP2, two nlp24-type PAMPs from the destructive fungal pathogen Sclerotinia sclerotiorum, activate two calcium-elicited kinases, CPK4 and CPK11, which phosphorylate WRKY8 and thus release its inhibition on RLP23 to promote accumulation of RLP23 transcripts. Meanwhile, SsNLPs activate the RLCK-type kinase PBL19, which phosphorylates WRKY8 and thus enhances accumulation of CERK1 transcripts. Intriguingly, RLP23 is repressed at later stage by PBL19-mediated phosphorylation of WRKY8, thus avoiding excessive immunity and enabling normal growth. Our findings unveil a plant strategy of "killing two birds with one stone" to elicit robust broad-spectrum immunity. This strategy is based on PAMP-triggered fine-tuning of a dual-role transcription factor to simultaneously amplify two PRRs that recognize PAMPs conserved across a wide range of pathogens. Moreover, our results reveal a novel plant strategy for balancing the trade-off between growth and immunity by fine-tuning the expression of multiple PRR genes.