Regulation of adenovirus alternative RNA splicing at the level of commitment complex formation (original) (raw)

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Department of Cell and Molecular Biology, The Medical Nobel Institute

Karolinska Instituted 171 77 Stockholm, Sweden

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Department of Cell and Molecular Biology, The Medical Nobel Institute

Karolinska Instituted 171 77 Stockholm, Sweden

* To whom correspondence should be addressed

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Received:

21 October 1993

Accepted:

20 December 1993

Published:

11 February 1994

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Jan-Peter Kreivi, Göran Akusjärvi, Regulation of adenovirus alternative RNA splicing at the level of commitment complex formation, Nucleic Acids Research, Volume 22, Issue 3, 11 February 1994, Pages 332–337, https://doi.org/10.1093/nar/22.3.332
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Abstract

The adenovirus late region 1 (L1) represents an example of an altenatively spliced gene where one 5′ splice site is spliced to two alternative 3′ splice sites, to produce two mRNAs; the 52,55K and Illa mRNAs, respectively. Accumulation of the L1 mRNAs is temporally regulated during the infectious cycle. Thus, the proximal 3′ splice site (52,55K mRNA) is used at all times during the infectious cycle whereas the distal 3′ splice site (Illa mRNA) is used exclusively late in infection. Here we show that in vitro splicing extracts prepared from late adenovirus-infected cells reproduces the virus-induced temporal shift from proximal to distal 3′ splice site selection in L1 pre-mRNA splicing. Two stable intermediates in spllceosome assembly have been identified; the commitment complex and the prespliceosome (or A complex). We show that the transition in splice site activity in L1 alternative splicing results from an increase in the efficiency of commitment complex formation using the distal 3′ splice site in extracts prepared from late virus-infected cells combined with a reduction of the efficiency of proximal 3′ splice site splicing. The increase in commitment activity on the distal 3′ splice site is paralleled by a virus-induced increase in A complex formation on the distal 3′ splice site. Importantly, the virus-induced shift from proximal to distal L1 3′ splice site usage does not require eis competition between the 52,55K and the Illa 3′ splice sites, but rather results from the intrinsic property of the two 3′ splice sites which make them respond differently to factors in extracts prepared from virus-infected cells.

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