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Regulation of adenovirus alternative RNA splicing at the level of commitment complex formation

J P Kreivi1, G Akusjärvi

  • 1Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institutet, Stockholm, Sweden.

Nucleic Acids Research
|February 11, 1994
PubMed

Insights

Adenovirus alternative splicing temporally regulates gene expression. During infection, the virus shifts 3' splice site selection in L1 pre-mRNA, favoring distal sites late in infection.

Area of Science:

  • Molecular Biology
  • Virology
  • Gene Regulation

Background:

  • Adenovirus late region 1 (L1) exhibits alternative splicing, producing 52,55K and IIIa mRNAs from a single 5' splice site and two alternative 3' splice sites.
  • L1 mRNA accumulation is temporally regulated during adenovirus infection, with proximal 3' splice site usage occurring throughout infection and distal 3' splice site usage exclusively late in infection.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the virus-induced temporal shift in 3' splice site selection in adenovirus L1 pre-mRNA splicing.
  • To determine if in vitro splicing extracts from infected cells can replicate the observed temporal regulation of splice site usage.

Main Methods:

  • Utilized in vitro splicing extracts prepared from adenovirus-infected cells.
  • Analyzed spliceosome assembly intermediates, specifically the commitment complex and pre-spliceosome (A complex).
  • Assessed the efficiency of splice site selection for both proximal and distal 3' splice sites.

Main Results:

  • In vitro splicing extracts from late adenovirus-infected cells reproduced the temporal shift in L1 3' splice site selection.
  • The shift is attributed to increased efficiency of commitment complex formation at the distal 3' splice site and reduced efficiency at the proximal site in late-infected cell extracts.
  • Virus-induced increases in A complex formation at the distal 3' splice site correlate with the shift in usage.
  • The observed shift does not depend on cis competition between the two 3' splice sites.

Conclusions:

  • Adenovirus infection alters the cellular splicing machinery to promote the use of the distal 3' splice site (IIIa mRNA) late in infection.
  • The temporal regulation of L1 alternative splicing is mediated by changes in the efficiency of spliceosome assembly intermediates, particularly commitment complex formation.
  • The intrinsic properties of the alternative 3' splice sites, rather than cis competition, dictate their differential usage in response to viral factors.

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