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J. Biol. Chem., Vol. 281, Issue 48, 36510-36517, December 1, 2006

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L4-33K, an Adenovirus-encoded Alternative RNA Splicing Factor^*>

From the Department of Medical Biochemistry and Microbiology, Uppsala University, S-751 23 Uppsala, Sweden

Splicing of the adenovirus IIIa mRNA is subjected to a strict temporal regulation during virus infection such that efficient IIIa 3' splice site usage is confined to the late phase of the infectious cycle. Here we show that the adenovirus L4-33K protein functions as a virus-encoded RNA splicing factor that preferentially activates splicing of transcripts with a weak 3' splice site sequence context, a sequence configuration that is shared by many of the late adenovirus 3' splice sites. Furthermore, we show that L4-33K activates IIIa splicing through the IIIa virus infection-dependent splicing enhancer element (3VDE). This element was previously shown to be the minimal element, both necessary and sufficient, for activation of IIIa splicing in the context of an adenovirus-infected cell. L4-33K stimulates an early step in spliceosome assembly and appears to be the only viral protein necessary to convert a nuclear extract prepared from uninfected HeLa cells to an extract with splicing properties very similar to a nuclear extract prepared from adenovirus late-infected cells. Collectively, our results suggest that L4-33K is the key viral protein required to activate the early to late switch in adenovirus major late L1 alternative splicing.

Received for publication, August 9, 2006 , and in revised form, October 5, 2006.

^* This work was supported by generous grants from the Swedish Cancer Society, the Wallenberg Consortium North, and EURASNET. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental data and references and Figs. 1 and 2.

¹ These authors contributed equally to this work.

² To whom correspondence should be addressed: Dept. of Medical Biochemistry and Microbiology, Uppsala University, BMC, Box 582, Husargatan 3, S-751 23 Uppsala, Sweden. Tel.: 46-18-471-4164; Fax: 46-18-50-98-76; E-mail: goran.akusjarvi{at}imbim.uu.se.

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