It is generally accepted that begomoviruses in the family Geminiviridae encode four proteins (from AC1/C1 to AC4/C4) using the complementary-sense DNA as template. Although AC5/C5 coding sequences are increasingly annotated in databases for many begomoviruses, the evolutionary relationships and functions of this putative protein in viral infection are obscure. In this study, the scientists in IPP-CAAS demonstrated several important functions of the AC5 protein of a bipartite begomovirus, Mungbean yellow mosaic India virus (MYMIV). Comparison of wild-type and ac5 mutant MYMIV viruses demonstrated that AC5 had a critical role in infection. Furthermore, they confirmed that AC5 activity affected symptom phenotypes, and suppressed both PTGS and TGS. The results demonstrated that MYMIV AC5 was a pathogenicity determinant and a potent RNA silencing suppressor that employed novel mechanisms to suppress antiviral defenses, and suggested that the AC5 function may be conserved among many begomoviruses.

The AC5 N-terminal domain suppresses post-transcriptional gene silencing (PTGS)

The AC5 C-terminal domain is responsible for transcriptional gene silencing (TGS) suppression, severe symptoms and necrotic responses

This work was supported by grants from the National NaturalScience Foundation of China (31390422 and U1136606), the National Key Basic Research and Development Program ofChina (2012CB114004) and the Zhejiang Provincial Natural Science Foundation for Outstanding Young Scientists (LR12C14001).

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