| Summary: | <p>Abstract</p> <p>Background</p> <p>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. In <it>Arabidopsis thaliana</it>, different ecotypes present varying susceptibilities to <it>Tobacco mosaic virus </it>strain U1 (TMV-U1). The rate of TMV-U1 systemic movement is delayed in ecotype Col-0 when compared with other 13 ecotypes.</p> <p>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.</p> <p>Results</p> <p>TMV-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 F<sub>1 </sub>and F<sub>2 </sub>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 <it>DSTM1 </it>(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.</p> <p>Conclusion</p> <p>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 TMV-U1 in this ecotype.</p>
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