Complex splicing patterns of RNAs from the early regions of adenovirus-2

Chow, Louise T.; Broker, Thomas R.; Lewis, James B.

doi:10.1016/0022-2836(79)90036-6

Cited by 542 publications

(384 citation statements)

References 77 publications

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“…First, the Ad12 54 kd and the Ad5 55 kd proteins are major El b gene products (Jochemsen, 1979;Schrier et al, 1979;Jochemsen et al, 1980;H. Jochemsen et al, submitted), and Sl nuclease analysis has shown that there is no other messenger available in appreciable amounts that could direct the synthesis of the 54-55 kd protein from the first AUG of the long open frame or, potentially, of a shorter peptide from an AUG triplet further downstream (Berk and Sharp, 1978;Chow et al, 1979Chow et al, , 1980Kitchingman and Westphal, 1980;Sawada and Fujinaga, 1980; this paper; P. J. van den Elsen and A. van der Eb, in preparation).…”

Section: Discussionmentioning

confidence: 99%

“…RNA mapping studies show that this region is divided into two transcription units, El a and El b (Flint, 1980). Most of the research on this transforming region has been directed at Ad2 and Ad5: the nucleotide sequence has been determined (van Ormondt et al, 1980b), the transcripts have been mapped (Berk and Sharp, 1978;Chow et al, 1979Chow et al, , 1980Kitchingman and Westphal, 1980) and the main gene products have been determined (Hatter and Lewis, 1978;Green et al, 1979;Halbert et al, 1979;Schrier et al, 1979;Ross et al, 1980;Jochemsen et al, 1981;Lupker et al, 1981). The combined evidence shows that the El a region encodes at least several proteins that are synthesized from overlapping RNAs differing by alternative splicing.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The 2.2 kb E1b mRNA of human Ad12 and Ad5 codes for two tumor antigens starting at different AUG triplets

Bos¹,

Polder²,

Bernards

et al. 1981

Cell

289

114

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The 2.2 kb E1b mRNA of human Ad12 and Ad5 codes for two tumor antigens starting at different AUG triplets

Bos¹,

Polder²,

Bernards

et al. 1981

Cell

289

114

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“…1). Thus, during the early phase of infection the MLP is active at a level comparable with the other early transcription units, whereas the same promoter accounts for most of the transcriptional activity at late times of infection (2,3). However, at early times transcription initiated at the MLP decreases gradually over a large region beginning after the L1 unit, with few RNA polymerases extending beyond the L3 polyadenylation sequence (4).…”

mentioning

confidence: 99%

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

Törmänen¹,

Backström²,

Carlsson

et al. 2006

Journal of Biological Chemistry

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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 lateinfected 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.Most late adenovirus proteins are translated from mRNAs originating from the major late transcription unit (MLTU), 3 which extends from the major late promoter (MLP) at coordinate 16.8 to a termination signal close to the right-hand end of the genome (reviewed in Ref. 1). The ϳ28,000-nucleotide pre-mRNA expressed from the MLTU becomes polyadenylated at one of five possible sites, generating five families of mRNAs with co-terminal 3Ј-ends (L1-L5; Fig. 1A). Following selection of a poly(A) site, the primary transcript is spliced in such a way that each mature mRNA receives a common set of three short 5Ј-leader segments, the tripartite leader (Fig. 1A). This leader is then spliced to one of several alternative 3Ј splice sites, generating a total of more than 20 cytoplasmic mRNAs.The accumulation of mRNA from the MLTU is subjected to a temporal regulation at the levels of transcription elongation, poly(A) site choice and alternative 3Ј splice site selection (reviewed in Ref. 1). Thus, during the early phase of infection the MLP is active at a level comparable with the other early transcription units, whereas the same promoter accounts for most of the transcriptional activity at late times of infection (2, 3). However, at early times transcription initiated at the MLP decreases gradually over a large region beginning after the L1 unit, with few RNA polymerases extending beyond the L3 polyadenylation sequence (4). At late times, this block in elongation is alleviated and transcripts initiated at the MLP continue to the right hand end of the genome. The control of MLTU transcription is further regulated by events taking place at the level of poly(A) and alternative 3Ј splice site selection (2, 5, 6). Thus, although nuclear transcription proceeds across at least the L1, L2 and L3 poly(A) sites a...

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“…At early times of infection, the E1A gene produces two transcripts, 12S and 13S in size, which encode products of 243 and 289 amino acids, respectively (Berk and Sharp 1978;Chow et al 1979;Perricaudet et al 1979;Kitchingman and Westphal 1980). Both products display regulatory activity; the product of 289 amino acids can trans-activate and repress gene transcription (Borrelli et al 1984;Velcich and Ziff 1985), whereas the protein of 243 amino acids, although it represses very efficiently (Borrelli et al 1984;Velcich and Ziff 1985), is generally found to be deficient in trans-activation (Carlock and Jones 1981;Montell et al 1982;Svensson and Akusjarvi 1984;Winberg and Shenk 1984;Lillie et al 1986;Moran et al 1986;Wu et al 1986a).…”

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confidence: 99%

Identification of factors that interact with the E1A-inducible adenovirus E3 promoter.

Hurst

Jones²

1987

Genes Dev.

185

195

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We have investigated the E1A-inducible E3 promoter of adenovirus type 5 with respect to its ability to bind specific nuclear proteins. Four distinct nucleoprotein-binding sites were detected, located between positions -7 to -33, -44 to -68, -81 to -103, and -154 to -183, relative to the E3 cap site. These sites contain sequences previously shown to be functionally important for efficient E3 transcription. No major qualitative or quantitative differences were found in the binding pattern between nucleoprotein extracts prepared from uninfected or adenovirus-infected HeLa cells. Competition experiments suggest that the factors binding to the -154 to -183 and -81 to -103 sites are the previously identified nucleoproteins, NFI and AP1, respectively. The factor binding to the -44 to -68 site, which we term ATF, also interacts with other E1A-inducible promoters and is very similar and probably identical to the factor that binds to the cAMP-responsive element of somatostatin. We have purified this factor, which is a protein of 43 kD in size.

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Complex splicing patterns of RNAs from the early regions of adenovirus-2

Cited by 542 publications

References 77 publications

The 2.2 kb E1b mRNA of human Ad12 and Ad5 codes for two tumor antigens starting at different AUG triplets

The 2.2 kb E1b mRNA of human Ad12 and Ad5 codes for two tumor antigens starting at different AUG triplets

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

Identification of factors that interact with the E1A-inducible adenovirus E3 promoter.

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