After infecting a plant cell, a Geminivirus starts to replicate (bottom right). This leads to the production of double stranded RNA molecules, which are processed by a DCL enzyme to produce virus-derived small interfering RNAs (vsiRNAs). These, in turn, trigger two defense mechanisms (black arrows) that aim to block virus replication. The vsiRNAs could be loaded into AGO1 and AGO2 enzymes to silence target viral mRNAs (known as post-transcriptional gene silencing), or could be loaded into AGO4 enzymes to direct DNA methylation (process called transcriptional gene silencing). KRYPTONITE (KYP), or another methyltranserase (MTase), methylates the histones in the viral minichromosome, which also promotes methylation of virus DNA. This results in the minichromosome becoming condensed, which blocks virus replication. However, many viruses produce suppressor proteins, such as TrAP, to counteract these defenses. TrAP blocks transcriptional gene silencing in two ways (red arrows): it inhibits the activity of the ADK enzyme leading to the accumulation of SAH (a molecule that blocks MTase activity) and a reduction in SAM (which is needed for methylation); TrAP can also directly bind to and inhibit the activity of KYP (and perhaps other MTases). Together these two process lead to the de-methylation of the minichromosome, which allows the virus to replicate. Abbreviations: DCL: Dicer-like ribonuclease; AGO: Argonaute; ADK: adenosine kinase; SAH: S-adenosylhomocysteine; SAM: S-adenosyl-methionine.