Transcriptional profiling of Arabidopsis defence responses to Cucumber mosaic virus

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Plants evolved complex defence systems against a range of abiotic and biotic stresses. The salicylic acid (SA), ethylene (ET), abscisic acid (ABA) and jasmonic acid (JA) pathways are the most researched defence systems. It is known that the various defence systems interact, but the specific factors that regulate these interactions are not thoroughly documented. This thesis addressed a range of physiological, biochemical and genetic tools to identify the genes activated in both compatible and incompatible plant-virus reactions. It also explored the relationships between these genes and other abiotic and biotic factors. Arabidopsis thaliana was infected with a compatible Australian isolate of Cucumber mosaic virus and used to determine the differentially expressed genes linked to plant defence pathways. These were compared to a documented incompatible virus reaction. Genes not previously associated with the compatible reaction were linked to the JA or ABA signalling response pathways. Regulatory genes of the SA pathway were expected to be differentially regulated in a virus response, but showed no significant change. ERF6, MYC2 and two NAC domain genes were identified as potential gene regulators of plant defence response pathways during this compatible reaction. Functional analysis of interactions between key genes revealed novel activation and suppression responses. In particular, the JA pathway regulator MYC2 was identified as a negative regulator of ERF6, a gene known to be involved in oxidative stress mitigation. Additionally, compatible virus assays across various mutant backgrounds in Arabidopsis supported the theory that the JA response pathway is activated by viral infection rather than the SA pathway. Other unexpected genes to show differentiation included those involved in the ABA response. Further investigation is warranted in order to determine if these genes are also involved in crosstalk of defence response pathways. The concept of pathway hijacking is known to occur in several plant pathogenic fungal and bacterial systems. This is the first record of several known regulatory genes in the JA pathway linked to successful virus infection. These data suggested upregulation of the JA pathway may have prevented SA signalling that could otherwise lead to virus resistance. Future work should focus on linking virus induced SA and JA pathways with the RNAi pathway during plant-virus interactions.