PRJNA560275
C.papaya transcriptome profiling reveals regulatory mechanisms of PapMV (Papaya mosaic virus) and PRSV (Papaya ringspot virus) antagonism
In natural environments, mixed viral infections are more a rule than an exception, with three types of interactions: antagonism, synergism and neutralism. In our system we report that the Papaya Mosaic virus (PapMV) and Papaya ringspot virus (PRSV) viruses can interact synergistically or antagonistically, depending on the order of infection, finding synergism when they infect both viruses at the same time or first infect PRSV. However, when it first infects PapMV and then PRSV, there is antagonism (Chávez-Calvillo, 2016). In this work, we seek to confirm whether the plant's immune system (innate or adaptive) is effectively involved in the antagonism response.In order to elucidate the possible molecular mechanisms involved in the antagonism, 12 libraries of cDNAs derived from RNAs from 12 libraries of control plants and plants with simple viral infections of each virus were sequenced, as well as mixed the three types of infection mixed that result in synergism or antagonism.1798 differentially expressed differentially genes were found for all conditions, as compared to control plants. For all conditions. Of these, 262 were expressed only in antagonism. The functional annotation of the genes was carried out with an enrichment analysis that resulted in 5 highly enriched ontology antagonisms: Defense response, Chitin response, Immune response, Response to carbohydrate stimuli and phospholipid biosynthetic process. Likewise, analyzes of metabolic pathways were performed and it was found that the path of plant-pathogen interaction is differentially expressed in antagonism.Currently, using RT-qPCR, the expression of 8 genes that can serve as a resource for further studies of the molecular mechanism involved in viral antagonism have been validated.In our work, it was described for the first time that in the antagonistic viral interaction the immune and defense response are the main mechanisms responsible for this phenotype