Localized control of cell death is crucial for the resistance of plants to pathogens. Papain-like cysteine proteases (PLCPs) regulate plant defence to drive cell death and protection against biotrophic pathogens. In maize (Zea mays)， PLCPs are crucial in the orchestration of salicylic acid (SA)-dependent defence signalling. Despite this central role in immunity， it remains unknown how PLCPs are activated， and which downstream signals they induce to trigger plant immunity. Here， we discover an immune signalling peptide， Z. mays immune signalling peptide 1 (Zip1)， which is produced after salicylic acid (SA) treatment. In vitro studies demonstrate that PLCPs are required to release bioactive Zip1 from ... More
Localized control of cell death is crucial for the resistance of plants to pathogens. Papain-like cysteine proteases (PLCPs) regulate plant defence to drive cell death and protection against biotrophic pathogens. In maize (Zea mays)， PLCPs are crucial in the orchestration of salicylic acid (SA)-dependent defence signalling. Despite this central role in immunity， it remains unknown how PLCPs are activated， and which downstream signals they induce to trigger plant immunity. Here， we discover an immune signalling peptide， Z. mays immune signalling peptide 1 (Zip1)， which is produced after salicylic acid (SA) treatment. In vitro studies demonstrate that PLCPs are required to release bioactive Zip1 from its propeptide precursor. Conversely， Zip1 treatment strongly elicits SA accumulation in leaves. Moreover， transcriptome analyses revealed that Zip1 and SA induce highly overlapping transcriptional changes. Consequently， Zip1 promotes the infection of the necrotrophic fungus Botrytis cinerea， while it reduces virulence of the biotrophic fungus Ustilago maydis. Thus， Zip1 represents the previously missing signal that is released by PLCPs to activate SA defence signalling.
