Research articleComparative proteomic and metabolomic studies between Prunus persica genotypes resistant and susceptible to Taphrina deformans suggest a molecular basis of resistance

- “Leaf curl disease” of stone fruits is world-wide distributed and caused by a fungus.
- Taphrina deformans is not detected in leaves of the resistant genotype.
- Protective proteins and compounds are constitutively present in resistant trees.
- Chlorogenic acid in vitro inhibits T. deformans growth.
- Chloroplasts are important site of plant defense responses against T. deformans.

The worldwide-distributed leaf peach curl disease is caused by the biotroph Taphrina deformans. To characterize the plant-fungus interaction, resistant and susceptible Prunus persica genotypes grown in the orchard were studied. Asymptomatic leaves were tested for fungal presence. In all resistant leaves analyzed the fungus was not detected. Conversely, leaves from the susceptible genotype were categorized according to the presence or absence of the pathogen.Comparative metabolomic analysis disclosed the metabolite composition associated with resistant and susceptible interactions, and of compounds involved in fungal growth inhibition such as chlorogenic acid, whose in vitro antifungal activity was verified in this work.Differential proteome studies revealed that chloroplasts are important site of plant defense responses against T. deformans. Members of the Bet-v1-like family protein differentially responded to the pathogen. Extracellular pathogenesis-related proteins, evaluated by qRT-PCR, and an enone oxidoreductase are constitutively present in leaves of resistant trees and could be related to fungal resistance.This study is a global view of the changes in the metabolome, proteome and transcripts related to plant defense in naturally infected leaves of susceptible plants during the asymptomatic stage. Additionally, it provides clues to the successful molecular mechanisms operating in resistant plants, which neither develop the disease nor harbor the pathogen.