Pepino mosaic virus (PepMV) is a plant pathogen distributed worldwide and mixed infections of the two prevailing PepMV strains are common in nature. PepMV mixed infections result in the repression of in planta accumulation of one of the strains, indicating a virus-virus antagonistic interaction.
A team of scientists have demonstrated that each strain causes specific transcriptomic alterations in the host. This contrasts with gene expression perturbations produced by mixed infections.
Genes which are critical in the RNA silencing pathway are differentially regulated by each strain, for example the AGO2 gene. Plants knocked-out in AGO2, are hypersusceptible to PepMV, although the loss of AGO2 alone does not change the phenotype of the virus-virus interaction.
PepMV is an RNA potexvirus that affects tomato crops worldwide, causing huge economic losses.
Two main strains co-circulate in PepMV epidemics: the CH2, which prevails, and the EU which is found mainly in mixed infections.
A research team showed previously that CH2 isolates have an increased in planta fitness compared to EU isolates during single infections. But, during mixed infections, the in planta fitness of CH2 isolates is reduced, defining an asymmetric antagonistic interaction between both viruses.
The authors of a recent article have studied the transcriptomic alterations of tomato plants in single or mixed infections with PepMV isolates of the EU and CH2 strains.
PepMV-EU and PepMV-CH2 modulate the tomato transcriptome in a strain-dependent manner, inducing deeper transcriptomic alterations at early infection times.
Comparing single and mixed PepMV infections; both caused similar transcriptomic perturbations at early infection times, but these clearly differed at later times post-infection.
Authors also showed that some host genes, likely involved in the antagonism between PepMV-EU and PepMV-CH2 in mixed infections, fulfil critical functions in the RNA silencing pathway, which is known to have a principal role controlling virus accumulation in the host and, hence, host susceptibility.
AGO and DCL genes were included in this group.
Then, plants with no expression of the AGO2 gene, were used to study the AGO2 role in PepMV infection. (These were Nicotiana benthamiana plants where the ago2 gene has been “knocked-out” of the genome, named ago2 plants.)
Higher accumulation of PepMV was found in ago2 plants compared with wild type plants, and in fact ago2 plants were hypersusceptible to PepMV. However, authors did not find any changes in the antagonistic interaction between PepMV-EU and PepMV-CH2 in ago2 plants, concluding that: although AGO2 plays a role in PepMV infection, it is not the direct or only determinant of the PepMV-EU and PepMV-CH2 antagonism, at least in N. benthamiana plants.
Cristina Alcaide, Livia Donaire and Miguel A. Aranda published this study in Molecular Plant Pathology: