Key result
Substitution of a single nonconsensus C or G at positions 22, 13, or 14 of the Rous sarcoma virus NRS diminished splicing suppression, whereas substitution of an A generated a preferred 5' splice site.
The Rous sarcoma virus NRS requires three nonconsensus uridines to effectively maintain unspliced RNA, functioning as a decoy 5' splice site.
Identifies key uridines for RSV NRS decoy function; leaves open extension to human retroviral splicing or therapies.
Rous sarcoma virus RNA contains a negative regulator of splicing (NRS) element that aids in maintenance of unspliced RNA. The NRS binds U1 snRNA at a sequence that deviates from the 5' splice site consensus by substitution of U's for A's at three positions: -2, +3, and +4. All three of these U's are important for NRS-mediated splicing suppression. Substitution of a single nonconsensus C or G at any of these sites diminished NRS activity, whereas substitution of a single A generated a preferred 5' splice site within the NRS.
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Paca et al. (2001) studied Rous sarcoma virus RNA splicing. NRS sequence mutations (U to A, C, or G at positions 22, 13, 14) vs. Wild-type NRS sequence was evaluated on Splicing from the myc 5' splice site (splicing suppression activity). Substitution of a single nonconsensus C or G at positions 22, 13, or 14 of the Rous sarcoma virus NRS diminished splicing suppression, whereas substitution of an A generated a preferred 5' splice site.
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