Viral Defense and Counterdefense: A Role for Adenosine Kinase in Innate Defense and RNA Silencing

Geminiviruses are single-stranded DNA viruses that cause severe disease (Figure 1) and considerable damage to crops worldwide, including tomato, cotton, maize, bean, and cassava. They have small circular genomes that lack genes for DNA and RNA polymerases, and viral replication and transcription are dependent on host plant enzymes. Many geminiviruses encode proteins, such as the AL2 protein from Tomato golden mosaic virus (TGMV) and L2 from Beet curly top virus (BCTV), that confer enhanced susceptibility to viral disease in host plants (Sunter et al., 2001). TGMV AL2 is a transcription factor necessary for the expression of late viral genes, but its ability to confer enhanced susceptibility apparently is not related to its transactivation function in viral gene expression. BCTV L2 is not required for viral gene expression and shares only limited identity with AL2 in a small region that might form a zinc binding domain. A number of studies have shown that AL2 and L2 function both to disable an innate metabolic defense pathway mediated by SNF1 kinase and to inhibit the adaptive RNA-silencing defense pathway in plants. In this issue of The Plant Cell , Wang et al. (pages 3020–3032) show that AL2 and L2 interact with and inactivate host plant adenosine kinase (ADK), a nucleoside kinase that may function in both the SNF1mediated and RNA-silencing defense pathways. The authors present evidence that AL2 and L2 inactivate ADK in infected plant cells and present hypotheses for the role of ADK in plant defense.