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Small RNAs

Antiviral RNAi in mammals

Nature Reviews Genetics volume 14, page 821 (2013)Cite this article

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One challenge of characterizing the roles for RNAi in mammalian cells is that the loss of key components of the RNAi machinery — such as the deletion of Dicer1 or of all four Argonaute (AGO) genes — is generally incompatible with cell and organism viability.

Maillard et al. took advantage of mouse embryonic stem cells (mESCs), which can survive these manipulations. The authors infected wild-type mESCs with encephalomyocarditis virus (EMCV); this virus has a single-stranded RNA (ssRNA) genome but produces long dsRNAs as part of its infection cycle. High-throughput RNA sequencing revealed that such infection resulted in the production of virus-derived 21–23-nucleotide small interfering RNAs (siRNAs), which are characteristic of the cleavage of long dsRNAs by mammalian DICER1. Indeed, Dicer1−/− mESCs failed to produce these siRNAs. Furthermore, biochemical analyses showed that these viral-derived siRNAs became bound by AGO2. Overall, these findings provide support that viral RNAs are processed by mammalian RNAi pathways as a putative antiviral mechanism.

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References

  1. Maillard, P. V. et al. Antiviral RNA interference in mammalian cells. Science 342, 235–238 (2013)

    Article  CAS  Google Scholar 

  2. Li, Y. et al. RNA interference functions as an antiviral immunity mechanism in mammals. Science 342, 231–234 (2013)

    Article  CAS  Google Scholar 

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  1. Darren J. Burgess
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Burgess, D. Antiviral RNAi in mammals. Nat Rev Genet 14, 821 (2013). https://doi.org/10.1038/nrg3616

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