Abstract
MicroRNAs (miRNAs) integrate with Argonaut (Ago) to create the RNA-induced silencing complex, and regulate gene expression by silencing target mRNAs. RNA editing of miRNA may affect miRNA processing, assembly of the Ago complex and target mRNA binding. However, the function of edited miRNA, assembled within the Ago complex, has not been extensively investigated. In this study, sequence analysis of the Ago complex of Marsupenaeus japonicus shrimp infected with white spot syndrome virus (WSSV) revealed that host ADAR (adenosine deaminase acting on RNA) catalysed A-to-I RNA editing of a viral miRNA (WSSV-miR-N12) at the +16 site. This editing of the non-seed sequence did not affect association of the edited miRNA with the Ago protein, but inhibited interaction between the miRNA and its target gene (wsv399). The WSSV early gene wsv399 inhibited WSSV infection. As a result, the RNA editing of miRNA caused virus latency. Our results highlight a novel example of miRNA editing in the miRNA-induced silencing complex.
Highlights
Post-transcriptional mechanisms play important roles in the regulation of gene expression
To investigate the miRNAs involved in antiviral immunity, shrimp were infected with white spot syndrome virus (WSSV), and the RNA contained within shrimp haemocyte Ago1 complexes was sequenced
The results revealed that the RNA editing of viral miRNA played an important role in the virus replication, showing the elaborate mechanism of virus replication regulated by miRNA. miRNAs have been reported to influence both virus replication and pathogenicity, and host innate antiviral immune responses [27]
Summary
Post-transcriptional mechanisms play important roles in the regulation of gene expression. RNA editing is one of the most important mechanisms of post-transcriptional genetic modification and generates a variety of cellular RNA signatures by base substitutions, insertions and deletions. The best characterized form of RNA editing found in mammals is base substitution of C to U (cytosine to uracil) and A to I (adenosine to inosine) [1]. The targets of ADARs are double-stranded regions of at least 15 –20 base pairs [4], and following A-to-I RNA editing, the translational machinery recognizes inosine (I) as guanosine (G), producing different protein isoforms. The RNA editing involved in forming the coding region of the glutamate receptor subunit GluR-B is a well-known example [5]. Bioinformatic analyses report that the majority of A ! I RNA editing sites exist in noncoding sequences, 50 and 30 untranslated regions (UTRs), intronic retrotransposon elements and repetitive sequences [7,8,9], and the role of the RNA editing in these regions is largely unknown
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