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Regulation of poly(A) site selection in adenovirus.

TitleRegulation of poly(A) site selection in adenovirus.
Publication TypeJournal Article
Year of Publication1989
AuthorsFalck-Pedersen E, Logan J
JournalJ Virol
Volume63
Issue2
Pagination532-41
Date Published1989 Feb
ISSN0022-538X
KeywordsAdenoviridae, Adenovirus Early Proteins, Genes, Regulator, Genes, Switch, Genes, Synthetic, Genes, Viral, Oncogene Proteins, Viral, Poly A, RNA Processing, Post-Transcriptional, RNA, Messenger, RNA, Viral, Transcription, Genetic
Abstract

We have investigated the mechanisms involved in the early-to-late RNA-processing switch which regulates the mRNA species generated from the adenovirus major late transcription unit (MLTU). In particular, polyadenylation choice mechanisms were characterized by using a reconstructed adenovirus E1A gene as a site for insertion of MLTU poly(A) regulation signals (L1 and L3). Adenovirus constructs containing the variant poly(A) recognition elements were used to compare E1A poly(A) signal utilization with wild-type MLTU (L1 to L5) utilization. In both early and late stages of infection, either polyadenylation site (L1 or L3) is capable of being utilized when presented as the only operational poly(A) site. In an early infection, a virus which contains multiple elements presented in tandem (L13) uses the first poly(A) site, L1, preferentially (ratio of L1 to L3, 8:1) in both E1A and MLTU loci. Transcription termination is not involved in restricting the utilization of the downstream L3 site. In a late infection, when each of the five MLTU poly(A) sites is used, a switch also occurs for the E1AL13 construct, with utilization of both the L1 and L3 poly(A) sites. The switch from early to late was not the result of altered processing factors in the late infection, as demonstrated by superinfecting the E1AL13 construct into cells which had already entered a late stage of infection. The superinfecting virus gave an L1-only phenotype; therefore, a cis mechanism is involved in adenovirus poly(A) regulation.

DOI10.1128/JVI.63.2.532-541.1989
Alternate JournalJ Virol
PubMed ID2562992
PubMed Central IDPMC247721

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