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  VIRUS-PLANT INTERACTIONS  

(last 5 years)

Effects of different Turnip mosaic virus strains on Arabidopsis Col-0 development.

Comparison of A buffer-inoculated, B JPN 1-infected and C UK1-infected plants. For better size and global architecture comparisons, pictures were taken with pots leaning to one side and plants were placed not to show creeping effects. D A JPN 1-infected plant showing the induced creeping effect. E A close-up of a UK 1-infected plant showing an extremely short flower stalkand flowers forming a bunch.

Bar = 5 cm.

For our studies of the interactions with higher plants, underlying or induced by the infection of viruses, we have mostly exploited over the last few years the pathosystem formed by the model plant Arabidopsis thaliana and Turnip mosaic virus (TuMV), a potyvirus. TuMV makes most of its proteins through the processing of a viral encoded polyprotein. During the past five years our results in this area have focused on the viral determinants of pathogenicity, the disease side of the viral infection, and the response of the infected plant to the infection by the virus.

 

Viruses are intracellular pathogens frequently inducing disease in the infected plant. Different viruses induce different diseases, this holding true even for different strains of the same virus. The combined use of viral infectious clones (cloned copies of viral genomes), mutagenesis, and genomic interchanges between different viruses or viral strains (chimeric viruses) allows the precise determination of viral pathogenicity determinants for specific disease symptoms. For TuMV the selection of virulent variants overcoming resistances that involve plant genes of the family of translation initiation factors, showed the involvement of the region coding for the viral genome-linked protein (VPg) in determining the specificity of the resistances. The results also suggest that the virulent TuMV variants could use an eIF4F-independent pathway, which would represent a novel pathway for potyviruses.
 

Two different TuMV strains were used to characterize the different symptomatology and strong differences in oxidative status induced by them. Early differences in several senescence-associated genes linked to specific regulatory networks were found, as well as persistent divergence in the production of reactive oxygen species (ROS) and scavenging systems. However, at a later stage, both strains induced nutrient competition, indicating that senescence rates are influenced by different mechanisms upon viral infections. It was also found that differential senescence progression and ROS accumulation between strains rely on an intact salicylic acid pathway.

Flower-stalk growth curves. Values represent averages of 6 to 14 plants per inoculum. UK 1 and JPN 1 represent wild-type Turnip mosaic virus inoculations. Ch. represent plants inoculated with chimeric viruses. Inoculation at 21 days post sowing, always before developmental stage 5. Open squares represent buffer-inoculated plants; filled squares, UK 1; filled circles, JPN 1; open circles, Ch.U(2511-3767)J; and triangles, Ch. J(2511-3767)U. Standard errors are shown.

TuMV infections also affect many plant developmental traits, an aspect which has not received much attention so far in plant-virus interactions studies. We found that the same two TuMV strains previously cited, differentially affect plant development including many developmental traits. One of these traits is flower stalk elongation. We have mapped the main component of this differential strain effect to the P3 cistron of the viral polyprotein, one of the most variable genomic regions in the virus genome. Transcriptomic and interactomic analyses at different stages of plant development revealed large differences in the number of genes affected by the different infections at medium infection times but no significant differences at very early times.

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