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A plant-infecting subviral RNA associated with poleroviruses produces a subgenomic RNA which resists exonuclease XRN1 in vitro
Subviral agents are nucleic acids which lack the features for classification as a virus. Tombusvirus-like associated RNAs (tlaRNAs) are subviral positive-sense, single-stranded RNAs that replicate autonomously, yet depend on a coinfecting virus for encapsidation and transmission. TlaRNAs produce abu...
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Published in: | Virology (New York, N.Y.) N.Y.), 2022-01, Vol.566, p.1-8 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Subviral agents are nucleic acids which lack the features for classification as a virus. Tombusvirus-like associated RNAs (tlaRNAs) are subviral positive-sense, single-stranded RNAs that replicate autonomously, yet depend on a coinfecting virus for encapsidation and transmission. TlaRNAs produce abundant subgenomic RNA (sgRNA) upon infection. Here, we investigate how the well-studied tlaRNA, ST9, produces sgRNA and its function. We found ST9 is a noncoding RNA, due to its lack of protein coding capacity. We used resistance assays with eukaryotic Exoribonuclease-1 (XRN1) to investigate sgRNA production via incomplete degradation of genomic RNA. The ST9 3’ untranslated region stalled XRN1 very near the 5’ sgRNA end. Thus, the XRN family of enzymes drives sgRNA accumulation in ST9-infected tissue by incomplete degradation of ST9 RNA. This work suggests tlaRNAs are not just parasites of viruses with compatible capsids, but also mutually beneficial partners that influence host cell RNA biology.
•Tombusvirus-like associated RNAs (TlaRNAs) produce an abundant noncoding sgRNA.•TlaRNA ST9 efficiently stalls RNA decay enzyme XRN1 at a site in its 3’ UTR.•ST9’s sgRNA is generated by incomplete degradation of the genomic RNA by XRN1.•ST9-XRN1 interaction implies subviral tlaRNAs may be viral partners vs. parasites. |
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ISSN: | 0042-6822 1096-0341 |
DOI: | 10.1016/j.virol.2021.11.002 |