Abstract
BackgroundViral infections and their spread throughout a plant require numerous interactions between the host and the virus. While new functions of viral proteins involved in these processes have been revealed, current knowledge of host factors involved in the spread of a viral infection is still insufficient. In Arabidopsis thaliana, different ecotypes present varying susceptibilities to Tobacco mosaic virus strain U1 (TMV-U1). The rate of TMV-U1 systemic movement is delayed in ecotype Col-0 when compared with other 13 ecotypes.We followed viral movement through vascular tissue in Col-0 plants by electronic microscopy studies. In addition, the delay in systemic movement of TMV-U1 was genetically studied.ResultsTMV-U1 reaches apical leaves only after 18 days post rosette inoculation (dpi) in Col-0, whereas it is detected at 9 dpi in the Uk-4 ecotype. Genetic crosses between Col-0 and Uk-4 ecotypes, followed by analysis of viral movement in F1 and F2 populations, revealed that this delayed movement correlates with a recessive, monogenic and nuclear locus. The use of selected polymorphic markers showed that this locus, denoted DSTM1 (Delayed Systemic Tobamovirus Movement 1), is positioned on the large arm of chromosome II. Electron microscopy studies following the virion's route in stems of Col-0 infected plants showed the presence of curved structures, instead of the typical rigid rods of TMV-U1. This was not observed in the case of TMV-U1 infection in Uk-4, where the observed virions have the typical rigid rod morphology.ConclusionThe presence of defectively assembled virions observed by electron microscopy in vascular tissue of Col-0 infected plants correlates with a recessive delayed systemic movement trait of TMV-U1 in this ecotype.
Highlights
Viral infections and their spread throughout a plant require numerous interactions between the host and the virus
The presence of defectively assembled virions observed by electron microscopy in vascular tissue of Col-0 infected plants correlates with a recessive delayed systemic movement trait of Tobacco mosaic virus strain U1 (TMV-U1) in this ecotype
We evaluated the systemic infection of TMV-U1 in fourteen ecotypes of Arabidopsis thaliana using in vitro grown plants [16]
Summary
Viral infections and their spread throughout a plant require numerous interactions between the host and the virus. While new functions of viral proteins involved in these processes have been revealed, current knowledge of host factors involved in the spread of a viral infection is still insufficient. Systemic viral infections in plants are complex processes that require compatible virus-host interactions in multiple tissues. These interactions include: viral genome replication in the cytoplasm of the initially infected cells, cellto-cell movement towards neighboring tissues, long-distance movement through the vascular tissue, phloem unloading and cell-to-cell movement in non-inoculated systemic tissues [1]. Recent studies have shown that replication and movement of viral complexes in infected tobacco tissues are strongly associated with plant structures such as the endoplasmic reticulum and the cytoskeleton [4,5,6]
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