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Substrate-dependent differences in U2AF requirement for splicing in adenovirus-infected cell extracts.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
2005 (English)In: J Biol Chem, ISSN 0021-9258, Vol. 280, no 27, 25478-84 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2005. Vol. 280, no 27, 25478-84 p.
Keyword [en]
Adenoviridae/*genetics, Adenoviridae Infections/*genetics/*metabolism, Cell Extracts, Hela Cells, Humans, Immunoglobulin M/genetics, Introns/physiology, Nuclear Proteins/*metabolism, RNA Precursors/*metabolism, RNA Splice Sites/physiology, RNA Splicing/*physiology, RNA; Small Nuclear/metabolism, Research Support; Non-U.S. Gov't, Ribonucleoproteins/*metabolism
Identifiers
URN: urn:nbn:se:uu:diva-80306PubMedID: 15899895OAI: oai:DiVA.org:uu-80306DiVA: diva2:108220
Available from: 2006-05-05 Created: 2006-05-05 Last updated: 2011-01-11
In thesis
1. Regulation of Adenoviral Gene Expression by the L4-33K and L4-22K Proteins
Open this publication in new window or tab >>Regulation of Adenoviral Gene Expression by the L4-33K and L4-22K Proteins
2009 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The splicing pattern during an adenovirus infection is shifted at the late phase towards using weaker splice sites, splicing out larger introns. Splicing of weak 3´ splice sites usually requires recognition of the 3´AG dinucleotide before the first catalytic step of splicing. Such splicing events are said to be AG-dependent and requires an interaction of both subunits of the cellular splicing factor U2AF with the 3´ splice site. We show that splicing of transcripts that are AG-dependent in uninfected nuclear extracts (NE) becomes AG-independent in nuclear extracts prepared form adenovirus late-infected HeLa cells (Ad-NE). Further we demonstrate that the first step in splicing of a model transcript, IgM, becomes completely U2AF-independent in Ad-NE. This finding supports our working model that 3´ splice site recognition in Ad-NE is altered, and in fact might be U2AF-independent.

We further show that the adenovirus late protein L4-33K acts as a virus encoded alternative splicing factor. L4-33K activates splicing of both cellular and viral transcripts containing weak 3´ splice sites. This supports the hypothesis that adenovirus alter splicing during the infection to favour usage of weak, suboptimal 3´ splice sites. However, we were unable to find an alternative U2AF-related factor that could stimulate L4-33K splicing enhancer activity. Furthermore, we demonstrate that the serine residues in the C-terminal part of L4-33K are important for the splicing enhancer activity but also for its nuclear localisation.

The adenovirus major late promoter is highly activated after the onset of viral genome replication. Protein complexes binding to downstream elements of the promoter are required for full enhancement of this promoter. We show that an L4-33K-related protein, L4-22K, stimulates transcription from the major late promoter. This stimulation is mainly via the downstream elements and does not require the viral IVa2 protein, which is a transcription factor of the major late promoter.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2009. 45 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 458
National Category
Microbiology in the medical area
Research subject
Medical Virology
Identifiers
urn:nbn:se:uu:diva-101324 (URN)978-91-554-7529-1 (ISBN)
Public defence
2009-06-04, C10:305, BMC, Husargatan 3, Uppsala, 09:15 (English)
Opponent
Supervisors
Available from: 2009-05-13 Created: 2009-04-22 Last updated: 2011-02-24Bibliographically approved

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PubMedhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=15899895&dopt=Citation

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Backström, EllenorAkusjärvi, Göran

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