The Arabidopsis thaliana onset of leaf death 12 mutation in the lectin receptor kinase P2K2 results in an autoimmune phenotype

Abstract

AbstractBackgroundPlant 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.ResultsHere, we characterized theonset of leaf death 12(old12) mutant that was identified in the Arabidopsis accession Landsbergerecta. Theold12mutant is characterized by a growth defect, spontaneous cell death, plant-defense gene activation, and early senescence. In addition, theold12phenotype is temperature reversible, thereby exhibiting all characteristics of an autoimmune mutant. Mapping the mutated locus revealed that theold12phenotype is caused by a mutation in theLectin Receptor Kinase P2-TYPE PURINERGIC RECEPTOR 2(P2K2) gene. Interestingly, the P2K2 allele from Landsbergerectais conserved amongBrassicaceae. P2K2 has been implicated in pathogen tolerance and sensing extracellular ATP. The constitutive activation of defense responses inold12results in improved resistance againstPseudomonas syringae pv. tomato DC3000.ConclusionWe demonstrate thatold12is an auto-immune mutant and that allelic variation ofP2K2contributes to diversity in Arabidopsis immune responses.