Geminivirus AL2 protein induces expression of, and interacts with, a calmodulin-like gene, an endogenous regulator of gene silencing.

RNA silencing is an innate cellular response involved in antiviral defense. Arabidopsis calmodulin-like protein 39 (At-rgsCaM) is related to known regulators of RNA silencing in tomato and Nicotiana tabacum. Geminivirus AL2 protein functions to suppress post-transcriptional and transcriptional gene silencing, possibly through induction of an endogenous regulator. In support of this, the At-rgsCaM promoter responds to Tomato golden mosaic virus (TGMV) AL2 in protoplasts and geminivirus infection increases rgsCaM expression in Arabidopsis and Nicotiana benthamiana. Further, over-expression of rgsCaM leads to increased susceptibility to infection, as a consequence of increased viral DNA loads. It has been shown that rgsCaM may target silencing suppressors of RNA viruses for degradation via the autophagy pathway. This interaction occurs within the cytoplasm, but AL2 interacts with rgsCaM in the nucleus. It is tempting to speculate that AL2 may act to sequester rgsCaM in the nucleus to prevent targeting of AL2 for degradation.