A nuclear translational block imposed by the HIV-1 U3 region is relieved by the Tat-TAR interaction

Braddock, Martin; Thorburn, Andrew; Chambers, A.; Elliott, Gillian; Anderson, Gordon J.; Kingsman, Alan J.; Kingsman, Susan M.

doi:10.1016/0092-8674(90)90389-v

Cited by 87 publications

(59 citation statements)

References 44 publications

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“…Tat with TAR has also been shown in special cases to enhance translation of genes transcribed from the HIV-1 LTR (Cullen 1986;Rosen et al 1986;Braddock et al 1989Braddock et al , 1990. Tat and N have similar arginine-rich domains that bind to cis-acting RNA sites, TAR and NUT, respectively (Lazinski et al 1989; Gait and Karn Cold Spring Harbor Laboratory Press on May 11, 2018 -Published by genesdev.cshlp.org Downloaded from 1993; Burd and Dreyfuss 1994), increasing the processivity of their respective polymerases.…”

Section: Discussionmentioning

confidence: 99%

Translational repression by a transcriptional elongation factor

Wilson¹,

Kameyama²,

Zhou³

et al. 1997

Genes Dev.

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Section: Discussionmentioning

confidence: 99%

Translational repression by a transcriptional elongation factor

Wilson¹,

Kameyama²,

Zhou³

et al. 1997

Genes Dev.

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“…Similar discrepancies have been reported previously and ascribed to post-transcriptional regulation by Tat (Cullen 1986;Feinberg et al 1986;Rosen et al 1986;Wright et al 1986). Recent studies have provided compelling evidence for a translational regulation by Tat in Xenopus oocytes (Braddock et al 1989(Braddock et al , 1990. Other workers, however, have failed to observe a post-transcriptional effect (Peterlin et al 1986;Jeang et al 1988;Rice and Mathews 1988a).…”

Section: ^^-^S^^^^^^x^n ^ ^ '^ ^ :H^mentioning

confidence: 99%

“…Tat produces a large stimulation of HIV-1-promoted RNA levels (CuUen 1986;Peterlin et al 1986;Wright et al 1986;Hauber et al 1987;Muesing et al 1987;Rice and Mathews 1988a) so the predominant mode of regulation appears to be transcriptional (Hauber et al 1987;Kao et al 1987;Jakobovits et al 1988;Jeang et al 1988;Rice and Mathews 1988a;Sadaie et al 1988;Laspia et al 1989), but evidence for posttranscriptional regulation also exists (Cullen 1986;Fein-Cold Spring Harbor Laboratory Press on April 4, 2019 -Published by genesdev.cshlp.org Downloaded from berg et al 1986;Rosen et al 1986;Wright et al 1986;Braddock et al 1989Braddock et al , 1990). In a model system consisting of replicating plasmids in COS cells, Kao et al (1987) found that Tat does not increase the initiation of transcription but act to stimulate transcriptional elongation.…”

mentioning

confidence: 99%

Synergy between HIV-1 Tat and adenovirus E1A is principally due to stabilization of transcriptional elongation.

Laspia¹,

Rice²,

Mathews³

1990

Genes & Development

107

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We studied the combined effects of Tat and general trans-activators, such as ElA and phorbol esters, on human immunodeficiency virus-1 (HIV-1) gene expression. Interaction between these two types of trans-activators may be involved in the transition from transcriptional quiesence during viral latency to active gene expression during productive infection. ElA cooperated with Tat to produce a fourfold greater increase in accumulation of full-length, cytoplasmic HIV-1-directed RNA than is expected if they were acting additively to increase RNA accumulation. Similarily, phorbol 12-myristate 13-acetate (PMA) also cooperated with Tat to elevate HIV RNA levels synergistically. Analysis of transcription rates across the HIV-1-directed transcription unit indicated, unexpectedly, that synergy between Tat and ElA could not be accounted for by increased promoter proximal transcription rates that were merely additive. However, Tat and ElA produced a greater than additive increase in transcription rates in the 3' end of the gene. These findings imply that synergy between Tat and ElA (or other general transcriptional activators) is due principally to stabilization of transcriptional elongation. Furthermore, the observation that Tat elicits only a small increase in promoter proximal transcription in the presence of ElA suggests that the magnitude of the effect of Tat on initiation is decreased when the basal level of transcription is increased. These findings underscore the importance of the ability of Tat to stabilize elongation, as well as to stimulate initiation, in an HIV-1-directed transcription unit.

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“…It was originally suggested by Braddock et al (1990) that a factor that blocks translation could be deposited on mRNA prior to export. In a similar vein, Bouvet and Wolffe (1994) showed that transcription is involved in relaying a negative translation factor to nascent RNA in the nucleus.…”

Section: Rna Nuclear and Cytoplasmic Regulationmentioning

confidence: 99%

The nuclear experience of CPEB: Implications for RNA processing and translational control

Lin¹,

Evans²,

Shen³

et al. 2009

RNA

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CPEB is a sequence-specific RNA binding protein that promotes polyadenylation-induced translation in early development, during cell cycle progression and cellular senescence, and following neuronal synapse stimulation. It controls polyadenylation and translation through other interacting molecules, most notably the poly(A) polymerase Gld2, the deadenylating enzyme PARN, and the eIF4E-binding protein Maskin. Here, we report that CPEB shuttles between the nucleus and cytoplasm and that its export occurs via the CRM1-dependent pathway. In the nucleus of Xenopus oocytes, CPEB associates with lampbrush chromosomes and several proteins involved in nuclear RNA processing. CPEB also interacts with Maskin in the nucleus as well as with CPE-containing mRNAs. Although the CPE does not regulate mRNA export, it influences the degree to which mRNAs are translationally repressed in the cytoplasm. Moreover, CPEB directly or indirectly mediates the alternative splicing of at least one pre-mRNA in mouse embryo fibroblasts as well as certain mouse tissues. We propose that CPEB, together with Maskin, binds mRNA in the nucleus to ensure tight translational repression upon export to the cytoplasm. In addition, we propose that nuclear CPEB regulates specific pre-mRNA alternative splicing.

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A nuclear translational block imposed by the HIV-1 U3 region is relieved by the Tat-TAR interaction

Cited by 87 publications

References 44 publications

Translational repression by a transcriptional elongation factor

Translational repression by a transcriptional elongation factor

Synergy between HIV-1 Tat and adenovirus E1A is principally due to stabilization of transcriptional elongation.

The nuclear experience of CPEB: Implications for RNA processing and translational control

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