Abstract
Previously described transgenic tobacco lines express the full length infectious Tobacco mosaic virus (TMV) genome under the 35S promoter (Siddiqui et al., 2007. Mol Plant Microbe Interact, 20: 1489–1494). Through their young stages these plants exhibit strong resistance against both the endogenously expressed and exogenously inoculated TMV, but at the age of about 7–8 weeks they break into TMV infection, with typical severe virus symptoms. Infections with some other viruses (Potato viruses Y, A, and X) induce the breaking of the TMV resistance and lead to synergistic proliferation of both viruses. To deduce the gene functions related to this early resistance, we have performed microarray analysis of the transgenic plants during the early resistant stage, and after the resistance break, and also of TMV-infected wild type tobacco plants. Comparison of these transcriptomes to those of corresponding wild type healthy plants indicated that 1362, 1150 and 550 transcripts were up-regulated in the transgenic plants before and after the resistance break, and in the TMV-infected wild type tobacco plants, respectively, and 1422, 1200 and 480 transcripts were down-regulated in these plants, respectively. These transcriptome alterations were distinctly different between the three types of plants, and it appears that several different mechanisms, such as the enhanced expression of the defense, hormone signaling and protein degradation pathways contributed to the TMV-resistance in the young transgenic plants. In addition to these alterations, we also observed a distinct and unique gene expression alteration in these plants, which was the strong suppression of the translational machinery. This may also contribute to the resistance by slowing down the synthesis of viral proteins. Viral replication potential may also be suppressed, to some extent, by the reduction of the translation initiation and elongation factors eIF-3 and eEF1A and B, which are required for the TMV replication complex.
Highlights
Viruses are obligate intracellular molecular parasites which depend on host’s cellular machinery and on multiple host factors to complete their infectious life cycle
Typical viral symptoms first appeared on upper leaves of the plants and slowly progressed towards the lower older leaves, i.e. showing similar symptom pattern as a normal Tobacco mosaic virus (TMV)-infection in wt tobacco plants
The results indicated that oxygen evolution was not changed much in the before resistance break (BRB) transgenic plants (Figure 5 A), whereas in after resistance break (ARB) and TMVi plants it was strongly reduced (Figure 5 B)
Summary
Viruses are obligate intracellular molecular parasites which depend on host’s cellular machinery and on multiple host factors to complete their infectious life cycle. Viruses can alter the functions and composition of their host cells to benefit their own proliferation They can enhance the expression of their needed host factors, bind or suppress various resistance factors, induce changes in the lipid composition of infected cells, and interfere with host’s hormonal pathways [1,8,13,20,21,22]. Viruses can initiate infection process only in susceptible host species that provide compatible host factors, needed for the viral replication and spread Many of these potential host species recognize the invading viruses and mount different defense mechanisms to stop their proliferation or spread. This may happen as a mere side-effect of the viral counter-defense, or as an active means to weaken hosts’ cellular status
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