Citrus leprosis is caused by citrus leprosis virus C (CiLV-C), transmitted by Brevipalpus yothersi mites, and is the main viral disease of citrus in Brazil. Differently from other plant viruses, CiLV-C is unable to accomplish systemic infection in its hosts, remaining restricted to cells around the inoculation sites, where symptoms of viral infection develop. Phenotypically, these features resemble the outcome a hypersensitivity response (HR) during an incompatible interaction. In fact, preliminary studies reported that CiLV-C infection induces the salicylic acid (SA) pathway, the expression of HR marker genes, the accumulation of reactive oxygen species and localized cell death, suggesting that the localized lesions caused by viral infection are a consequence of an HR. Further analysis revealed that CiLV-C P61 protein mimicries the responses observed during plant-virus interaction, indicating P61 as the viral component that elicits the plant immune system and the consequent development of the disease symptoms. Even tough recent reports predict P61 as a virion glycoprotein and subcellular localization studies show that the protein triggers the remodeling of the endoplasmic reticulum (ER), the P61 function remains unknown. Here, we propose the biochemical and function characterization of P61 to unravel its role as a pathogenicity determinant of CiLV-C. We aim to confirm the elicitor activity of P61, to clarify the role of SA in the development of the induced HR, to identify P61 structural motifs and/or functional domains involved in the induction of this phenotype, to verify the occurrence of ER stress in response to P61 expression, to unravel the plant proteins that interacts with P61 to trigger the plant immune system, and to determine the P61 involvement as integral part of the virion envelope. The generated results will contribute to a better understanding of the pathosystem and to the establishment of more sustainable strategies of disease control.
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