Tobacco mosaic virus - induced alterations in the transcriptional profile of Arabidopsis thaliana: Effects on symptom development

Virus infections cause abberations in host physiological processes by altering the transcriptional patterns of the host. To identify changes in the host transcriptome in response to Tobacco Mosaic Virus infection, Arabidopsis leaf tissues infected with TMV were subjected to expression profiling using cDNA microarrays. As a result, a number of genes expressing functionally diverse proteins were found to display significant alterations in expression patterns, suggesting that TMV infection may impact a variety of host biochemical processes. The identified genes were used in the construction of a virus-specific microarray that can be used for studying the finer details of TMV disease process.; Further studies involved understanding the molecular aspects of symptom development in TMV infection using an attenuated strain of TMV. Characterization of the attenuated virus using functional assays and the virus-specific microarray suggested that differential regulation of genes coding for certain transcription factors and metabolic enzymes, and interactions between virus- and host-encoded components may contribute to the physiological alterations underlying symptom development. Yeast-2-hybrid assays were performed to identify potential interactions between virus and host components. Results indicated that the viral helicase domain interacts with several host proteins, suggesting a possible role for these interactions in disease development. These studies in conjunction with microarray analysis of the host transcriptome in response to WT-TMV infection led to a hypothesis linking the interaction between the viral helicase domain and a host catalase 3-like protein to necrotic symptoms observed in Arabidopsis tissues inoculated with TMV. To test this hypothesis, the putative helicase-catalase interaction was further investigated. Results suggest that necrosis observed in TMV-infected Arabidopsis may be partially attributed to the interaction between the helicase domain and catalase-like protein; this interaction may perhaps be one among a complex network of virus-host associations that are involved in the development of disease symptoms.