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Viruses 2017, 9(8), 204; doi:10.3390/v9080204

Rous Sarcoma Virus RNA Stability Element Inhibits Deadenylation of mRNAs with Long 3′UTRs

Biology Department, Johns Hopkins University, Baltimore, MD 21218, USA
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Academic Editor: Eric O. Freed
Received: 5 June 2017 / Revised: 14 July 2017 / Accepted: 26 July 2017 / Published: 1 August 2017
(This article belongs to the Special Issue Viral Interactions with Host RNA Decay Pathways)
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Abstract

All retroviruses use their full-length primary transcript as the major mRNA for Group-specific antigen (Gag) capsid proteins. This results in a long 3′ untranslated region (UTR) downstream of the termination codon. In the case of Rous sarcoma virus (RSV), there is a 7 kb 3′UTR downstream of the gag terminator, containing the pol, env, and src genes. mRNAs containing long 3′UTRs, like those with premature termination codons, are frequently recognized by the cellular nonsense-mediated mRNA decay (NMD) machinery and targeted for degradation. To prevent this, RSV has evolved an RNA stability element (RSE) in the RNA immediately downstream of the gag termination codon. This 400-nt RNA sequence stabilizes premature termination codons (PTCs) in gag. It also stabilizes globin mRNAs with long 3′UTRs, when placed downstream of the termination codon. It is not clear how the RSE stabilizes the mRNA and prevents decay. We show here that the presence of RSE inhibits deadenylation severely. In addition, the RSE also impairs decapping (DCP2) and 5′-3′ exonucleolytic (XRN1) function in knockdown experiments in human cells. View Full-Text
Keywords: Rous sarcoma virus; RNA stability element; nonsense mediated decay; long 3′UTR; deadenylation; decapping Rous sarcoma virus; RNA stability element; nonsense mediated decay; long 3′UTR; deadenylation; decapping
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MDPI and ACS Style

Balagopal, V.; Beemon, K.L. Rous Sarcoma Virus RNA Stability Element Inhibits Deadenylation of mRNAs with Long 3′UTRs. Viruses 2017, 9, 204.

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