| Geminivirus AL2 and L2 proteins cause enhanced susceptibility when expressed in transgenic plants, characterized primarily by an increase in viral infectivity. Here we present genetic and biochemical evidence which indicates that enhanced susceptibility is due to the interaction of AL2 and L2 with SNF1 kinase, a global regulator of metabolism. Specifically, we show that AL2 and L2 inactivate SNF1 in vitro and in vivo. We further demonstrate that expression of an antisense SNF1 transgene in Nicotiana benthamiana plants causes enhanced susceptibility similar to that conditioned by the AL2 and L2 transgenes, while SNF1over-expression leads to enhanced resistance. Transgenic plants expressing an AL2 protein lacking a significant portion of the SNF1 interaction domain do not display enhanced susceptibility. Together, these observations suggest that the metabolic alterations mediated by SNF1 are a component of innate antiviral defenses, and that SNF1 inactivation by AL2 and L2 is a counterdefensive measure. They also indicate that geminiviruses are able to modify host metabolism to their own advantage, and provide a molecular link between metabolic status and inherent susceptibility to viral pathogens. |
