Background: At the moment, there are a number of publications describing gene expression profiling in virus-infected plants. Most of the data are limited to specific host-pathogen interactions involving a given virus and a model host plant - usually Arabidopsis thaliana. Even though several summarizing attempts have been made, a general picture of gene expression changes in susceptible virus-host interactions is lacking.
Methods: To analyze transcriptome response to virus infection, we have assembled currently available microarray data on changes in gene expression levels in compatible Arabidopsis-virus interactions. We used the mean r (Pearson's correlation coefficient) for neighboring pairs to estimate pairwise local similarity in expression in the Arabidopsis genome.
Results: Here we provide a functional classification of genes with altered expression levels. We also demonstrate that responsive genes may be grouped or clustered based on their co-expression pattern and chromosomal location.
Conclusions: In summary, we found that there is a greater variety of upregulated genes in the course of viral pathogenesis as compared to repressed genes. Distribution of the responsive genes in combined viral databases differed from that of the whole Arabidopsis genome, thus underlining a role of the specific biological processes in common mechanisms of general resistance against viruses and in physiological/cellular changes caused by infection. Using integrative platforms for the analysis of gene expression data and functional profiling, we identified overrepresented functional groups among activated and repressed genes. Each virus-host interaction is unique in terms of the genes with altered expression levels and the number of shared genes affected by all viruses is very limited. At the same time, common genes can participate in virus-, fungi- and bacteria-host interaction. According to our data, non-homologous genes that are located in close proximity to each other on the chromosomes, and whose expression profiles are modified as a result of the viral infection, occupy 12% of the genome. Among them 5% form co-expressed and co-regulated clusters.