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. 2017 Sep 20;8:1801. doi: 10.3389/fmicb.2017.01801

FIGURE 3.

FIGURE 3

Model for the regulation of the AGO1 mRNA level mediated by tombusviral protein P19-induced miR168. The AGO1 protein plays a central role in plant defensive response against pathogens, and viral infection induces enhanced expression of AGO1 mRNA. Meanwhile, the virus produces the P19 VSR. P19 forms head-to-tail homodimers that bind to virus-encoded siRNAs (vsiRNAs), siRNAs and endogenous miRNAs with high affinity, preventing their loading into AGO1. However, miR168 is not efficiently bound by P19, resulting in the increased loading of miR168 into AGO1. Because miR168 directly represses the AGO1 mRNA, the accumulation of antiviral AGO1 is sharply decreased. In addition, tombusvirus infection also stimulates MIR168 transcription, and the expression of AGO1 mRNA is consequently further repressed by the increased miR168 level. Therefore, P19 VSR can not only sequester small RNAs, but can also effectively inhibit the loading of viral siRNAs onto AGO1.