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Plant pathogens with a broad host range are able to infect plant lineages that diverged over 100 million years ago. They exert similar and recurring constraints on the evolution of unrelated plant populations. Plants generally respond with quantitative disease resistance (QDR), a form of immunity relying on complex genetic determinants. In most cases, the molecular determinants of QDR and how they evolve is unknown. Here we identify in  Arabidopsis thaliana  a gene mediating QDR against  Sclerotinia sclerotiorum , agent of the white mold disease, and provide evidence of its convergent evolution in multiple plant species. Using genome wide association mapping in  A .  thaliana , we associated the gene encoding the POQR prolyl-oligopeptidase with QDR against  S .  sclerotiorum . Loss of this gene compromised QDR against  S .  sclerotiorum  but not against a bacterial pathogen. Natural diversity analysis associated  POQR  sequence with QDR. Remarkably, the same amino acid changes occurred after independent duplications of  POQR  in ancestors of multiple plant species, including  A .  thaliana  and tomato. Genome-scale expression analyses revealed that parallel divergence in gene expression upon  S .  sclerotiorum  infection is a frequent pattern in genes, such as  POQR , that duplicated both in  A .  thaliana  and tomato. Our study identifies a previously uncharacterized gene mediating QDR against  S .  sclerotiorum . It shows that some QDR determinants are conserved in distantly related plants and have emerged through the repeated use of similar genetic polymorphisms at different evolutionary time scales.

Parallel evolution of the POQR prolyl oligo peptidase gene conferring plant quantitative disease resistance