Loss of PR1 function enhances Arabidopsis resistance to Botrytis cinerea

PATHOGENESIS-RELATED 1 (PR1) is one of the most widely used markers of salicylic acid (SA)-dependent plant immunity, yet its direct functional contribution to pathogen defence remains poorly understood. Here, we investigated the role of PR1 in Arabidopsis thaliana by analyzing a pr1 loss-of-function mutant challenged with bacterial and fungal pathogens and fumonisin B1 (FB1)-induced cell death. Notably, loss of PR1 led to markedly different responses to distinct pathogens; while it moderately increased susceptibility to the pathogenic bacterium Pseudomonas syringae, it substantially enhanced resistance to the necrotrophic fungus Botrytis cinerea, and the responses to the necrotroph Sclerotinia sclerotiorum remained unaltered. The pr1 mutant also displayed reduced spread of FB1-induced cell death, linking PR1 function to the promotion of stress-associated cell death. In line with the susceptibility changes, we observed the strongest PR1 accumulation and cell wall enrichment during B. cinerea infection using mCherry-tagged PR1 expressed under its endogenous promoter. Complementation with full-length PR1 and with a C-terminally truncated PR1 variant lacking the CAPE peptide restored wild-type susceptibility, whereas a non-cleavable PR1 variant did not. These results indicate that proteolytic processing at the CAPE cleavage motif, rather than the CAPE peptide itself, is required for PR1 function. Our data thus strongly suggest that PR1 may act as a susceptibility factor for necrotrophic pathogens by promoting host cell death.