Abstract
In the past, we showed that local infection of tobacco leaves with either tobacco mosaic virus or oilseed rape mosaic virus (ORMV) resulted in a systemic increase in the homologous recombination frequency (HRF). Later on, we showed that a similar phenomenon occurs in Arabidopsis thaliana plants infected with ORMV. Here, we tested whether the time of removing the infected leaves as well as viral titer have any effect on the degree of changes in HRF in systemic tissues. An increase in HRF in systemic non-infected tissues was more pronounced when the infected leaves were detached from the infected plants at 60–96 h post-infection, rather than at earlier time. Next, we found that exposure to higher concentrations of inoculum was much more efficient in triggering an increase in HRF than exposure to lower concentrations. Finally, we showed that older plants exhibited a higher increase in HRF than younger plants. We found that an increase in genome instability in systemic tissues of locally infected plants depends on plant age, the concentration of initial inoculums and the time of viral replication.
Highlights
Viral infection is a common stress for plants
While analyzing homologous recombination frequency (HRF) in plants infected with 50, 100, or 200 ng of oilseed rape mosaic virus (ORMV) (the infected leaves were removed at 48 hpi, we found that HRF was the highest in plants infected with 200 ng and the lowest in those ones infected with 50 ng ORMV (Figure 1)
Since the previous experiment showed that the highest concentration of primary inoculums resulted in the highest increase in HRF, we hypothesized that an increase in HRF is more or less proportional to the amount of viral RNA initially encountered by plants
Summary
Viral infection is a common stress for plants. Typically, plants respond to such attack by activating various defense pathways. The recognition of a pathogen through gene-for-gene interactions results in an incompatible response that manifests itself in the salicylic acid (SA)-dependent restriction of virus movement and the activation of systemic defense against future pathogen attacks known as systemic acquired resistance (Durrant and Dong, 2004; Scholthof, 2004). If either the R-gene or the Avrgene is missing, interactions between pathogens and plants are compatible; viruses are able to spread and infect plants systemically (Dong, 2001; Scholthof, 2004). Incompatible interactions between TMV/ORMV and tobacco cultivar Big Havana plants that have the gene of resistance against these viruses did not result in an increase in HRF (Kovalchuk et al, 2003). We hypothesized that a compatible interaction triggers the production of a systemic signal that spreads faster than a virus and promotes an increase in HRF in non-infected tissues
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