Abstract
MicroRNAs (miRNAs) are a ubiquitous component of gene regulatory networks that modulate the precise amounts of proteins expressed in a cell. Despite their small size, miRNA genes contain various recognition elements that enable specificity in when, where and to what extent they are expressed. The importance of precise control of miRNA expression is underscored by functional studies in model organisms and by the association between miRNA mis-expression and disease. In the last decade, identification of the pathways by which miRNAs are produced, matured and turned-over has revealed many aspects of their biogenesis that are subject to regulation. Studies in viral systems have revealed a range of mechanisms by which viruses target these pathways through viral proteins or non-coding RNAs in order to regulate cellular gene expression. In parallel, a field of study has evolved around the activation and suppression of antiviral RNA interference (RNAi) by viruses. Virus encoded suppressors of RNAi can impact miRNA biogenesis in cases where miRNA and small interfering RNA pathways converge. Here we review the literature on the mechanisms by which miRNA biogenesis and turnover are regulated in animals and the diverse strategies that viruses use to subvert or inhibit these processes.
Highlights
Small RNA classificationThe specific recognition of nucleic acid sequences by RNA–protein complexes (RNPs) is central to transcriptional and post-transcriptional gene regulation
Each class of small RNAs binds to a member of the Argonaute (Ago) family of proteins: short interfering RNAs (siRNAs) and miRNAs associate with the Ago clade, whereas piwiinteracting RNAs (piRNAs) associate with the Piwi clade, reviewed in [4]
The RNA-induced silencing complex (RISC) containing miRNAs are found throughout the eukaryal domain and primarily target messenger RNAs, causing the inhibition of translation and/or de-adenylation and degradation of the mRNAs, reviewed in [6]
Summary
The specific recognition of nucleic acid sequences by RNA–protein complexes (RNPs) is central to transcriptional and post-transcriptional gene regulation. Like Lin, KSRP and TDP-43 are involved in both pri- and pre-miRNA processing but they serve to promote, rather than inhibit, processing (Fig. 1b, d) [60, 63] These findings suggest that the terminal loop is an important platform for both ‘‘activators’’ (for example, hnRNP A1, KSRP and TDP-43) and ‘‘repressors’’ (for example, Lin28) to modulate miRNA levels and thereby gene regulation, reviewed in [109]. This mechanism provides a route for viral miRNA biogenesis that does not result in cleavage of the retroviral genomic RNA [18]. The A to I conversion within the mature miRNA can retarget the miRNA to a new set of
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