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The structure and function of the rous sarcoma virus RNA stability element
Author(s) -
Withers Johanna B.,
Beemon Karen L.
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23272
Subject(s) - rous sarcoma virus , rna , rna splicing , biology , messenger rna , nuclear export signal , microbiology and biotechnology , virus , virology , gene , genetics
For simple retroviruses, such as the Rous sarcoma virus (RSV), post‐transcriptional control elements regulate viral RNA splicing, export, stability, and packaging into virions. These RNA sequences interact with cellular host proteins to regulate and facilitate productive viral infections. One such element, known as the RSV stability element (RSE), is required for maintaining stability of the full‐length unspliced RNA. This viral RNA serves as the mRNA for the Gag and Pol proteins and also as the genome packaged in progeny virions. When the RSE is deleted from the viral RNA, the unspliced RNA becomes unstable and is degraded in a Upf1‐dependent manner. Current evidence suggests that the RSE inhibits recognition of the viral gag termination codon by the nonsense‐mediated mRNA decay (NMD) pathway. We believe that the RSE acts as an insulator to NMD, thereby preventing at least one of the required functional steps that target an mRNA for degradation. Here, we discuss the history of the RSE and the current model of how the RSE is interacting with cellular NMD factors. J. Cell. Biochem. 112: 3085–3092, 2011. © 2011 Wiley Periodicals, Inc.