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BACKGROUND: Plant immunity relies on the perception of immunogenic signals by cell-surface and intracellular receptors and subsequent activation of defense responses like programmed cell death. Under certain circumstances, the fine-tuned innate immune system of plants results in the activation of autoimmune responses that cause constitutive defense responses and spontaneous cell death in the absence of pathogens.; RESULTS: Here, we characterized the onset of leaf death 12 (old12) mutant that was identified in the Arabidopsis accession Landsberg erecta. The old12 mutant is characterized by a growth defect, spontaneous cell death, plant-defense gene activation, and early senescence. In addition, the old12 phenotype is temperature reversible, thereby exhibiting all characteristics of an autoimmune mutant. Mapping the mutated locus revealed that the old12 phenotype is caused by a mutation in the Lectin Receptor Kinase P2-TYPE PURINERGIC RECEPTOR 2 (P2K2) gene. Interestingly, the P2K2 allele from Landsberg erecta is conserved among Brassicaceae. P2K2 has been implicated in pathogen tolerance and sensing extracellular ATP. The constitutive activation of defense responses in old12 results in improved resistance against Pseudomonas syringae pv. tomato DC3000.; CONCLUSION: We demonstrate that old12 is an auto-immune mutant and that allelic variation of P2K2 contributes to diversity in Arabidopsis immune responses. © 2023. The Author(s).

Additional file 1: Fig. S1. Early-senescence phenotype of old12 under short-day condition. Fig. S2. Visualization of allele frequency by SHOREmap. Fig. S3. Absence of old12 phenotype in p2k2-1. Fig. S4. Comparison of the protein sequence of P2K2 from different accessions. Fig. S5. Conservation of the C-terminal extension of P2K2 in Brassicaceae. Fig. S6. Full blot images for figure 4 Fig. S7. Tissue-specific expression of P2K2 in Col-0. Fig. S8. Crossing of npr1 into the old12 mutant results in leaf bleaching. Table S1. Putative EMS-induced SNPs on Chromosome I. Table S2. qPCR primers used.