Evidence that a threshold of serine/arginine-rich (SR) proteins recruits CFIm to promote rous sarcoma virus mRNA 3' end formation. Virology 2016 Nov;498:181-191
Date
09/07/2016Pubmed ID
27596537Pubmed Central ID
PMC5045808DOI
10.1016/j.virol.2016.08.021Scopus ID
2-s2.0-84985990676 (requires institutional sign-in at Scopus site) 3 CitationsAbstract
The weak polyadenylation site (PAS) of Rous sarcoma virus (RSV) is activated by the juxtaposition of SR protein binding sites within the spatially separate negative regulator of splicing (NRS) element and the env RNA splicing enhancer (Env enhancer), which are far upstream of the PAS. Juxtaposition occurs by formation of the NRS - 3' ss splicing regulatory complex and is thought to provide a threshold of SR proteins that facilitate long-range stimulation of the PAS. We provide evidence for the threshold model by showing that greater than three synthetic SR protein binding sites are needed to substitute for the Env enhancer, that either the NRS or Env enhancer alone promotes polyadenylation when the distance to the PAS is decreased, and that SR protein binding sites promote binding of the polyadenylation factor cleavage factor I (CFIm) to the weak PAS. These observations may be relevant for cellular PASs.
Author List
Hudson SW, McNally LM, McNally MTAuthor
Mark T. McNally PhD Associate Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBinding Sites
Cell Line
Gene Order
Open Reading Frames
Poly A
Polyadenylation
Protein Binding
RNA, Messenger
RNA, Viral
RNA-Binding Proteins
Rous sarcoma virus
mRNA Cleavage and Polyadenylation Factors
