Label-free quantitative proteomic analysis of pre-flowering PMeV-infected Carica papaya L.

Papaya meleira virus (PMeV) infects papaya (Carica papaya L.) and leads to Papaya Sticky Disease (PSD) or "Meleira", characterized by a spontaneous exudation of latex from fruits and leaves only in the post-flowering developmental stage. The latex oxidizes in contact with air and accumulates as a sticky substance on the plant organs, impairing papaya fruit's marketing and exportation. To understand pre-flowering C. papaya resistance to PMeV, an LC-MS/MS-based label-free proteomics approach was used to assess the differential proteome of PMeV-infected pre-flowering C. papaya vs. uninfected (control) plants. In this study, 1333 proteins were identified, of which 111 proteins showed a significant abundance change (57 increased and 54 decreased) and supports the hypothesis of increased photosynthesis and reduction of 26S-proteassoma activity and cell-wall remodeling. All of these results suggest that increased photosynthetic activity has a positive effect on the induction of plant immunity, whereas the reduction of caspase-like activity and the observed changes in the cell-wall associated proteins impairs the full activation of defense response based on hypersensitive response and viral movement obstruction in pre-flowering C. papaya plants. BIOLOGICAL SIGNIFICANCE: The papaya (Carica papaya L.) fruit's production is severely limited by the occurrence of Papaya meleira virus (PMeV) infection, which causes Papaya Sticky Disease (PSD). Despite the efforts to understand key features involved with the plant×virus interaction, PSD management is still largely based on the observation of the first disease symptoms in the field, followed by the elimination of the diseased plants. However, C. papaya develops PSD only after flowering, i.e. about six-months after planting, and the virus inoculum sources are kept in field. The development of PMeV resistant genotypes is impaired by the limited knowledge about C. papaya resistance against viruses. The occurrence of a resistance/tolerance mechanism to PSD symptoms development prior to C. papaya flowering is considered in this study. Thus, field-grown and PMeV-infected C. papaya leaf samples were analyzed using proteomics, which revealed the modulation of photosynthesis-, 26S proteasome- and cell-wall remodeling-associated proteins. The data implicate a role for those systems in C. papaya resistance to viruses and support the idea of a partial resistance induction in the plants at pre-flowering stage. The specific proteins presented in the manuscript represent a starting point to the selection of key genes to be used in C. papaya improvement to PMeV infection resistance. The presented data also contribute to the understanding of virus-induced disease symptoms development in plants, of interest to the plant-virus interaction field.