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Titolo:
THE EXON SPLICING SILENCER IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TATEXON-3 IS BIPARTITE AND ACTS EARLY IN SPLICEOSOME ASSEMBLY
Autore:
SI ZH; RAUCH D; STOLTZFUS CM;
Indirizzi:
UNIV IOWA,DEPT MICROBIOL,3770 BOWEN SCI BLDG IOWA CITY IA 52242 UNIV IOWA,DEPT MICROBIOL IOWA CITY IA 52242
Titolo Testata:
Molecular and cellular biology
fascicolo: 9, volume: 18, anno: 1998,
pagine: 5404 - 5413
SICI:
0270-7306(1998)18:9<5404:TESSIH>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRE-MESSENGER-RNA; ROUS-SARCOMA VIRUS; BRANCH SITE; NUCLEAR RIBONUCLEOPROTEINS; RETROVIRUS RNA; UNSPLICED RNA; IN-VITRO; EXPRESSION; PROTEIN; REPLICATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
52
Recensione:
Indirizzi per estratti:
Citazione:
Z.H. Si et al., "THE EXON SPLICING SILENCER IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TATEXON-3 IS BIPARTITE AND ACTS EARLY IN SPLICEOSOME ASSEMBLY", Molecular and cellular biology, 18(9), 1998, pp. 5404-5413

Abstract

Inefficient splicing of human immunodeficiency virus type 1 (HIV-1) RNA is necessary to preserve unspliced and singly spliced viral RNAs for transport to the cytoplasm by the Rev-dependent pathway. Signals within the HIV-1 genome that control the rate of splicing include weak 3'splice sites, exon splicing enhancers (ESE), and exon splicing silencers (ESS). We have previously shown that an ESS present within tat exon 2 (ESS2) and a suboptimal 3' splice site together act to inhibit splicing at the 3' splice site flanking tat exon 2. This occurs at an early step in spliceosome assembly. Splicing at the 3' splice site flanking tat exon 3 is regulated by a bipartite element composed of an ESE and an ESS (ESS3). Here we show that ESS3 is composed of two smaller elements (AGAUCC and UUAG) that can inhibit splicing independently. We also show that ESS3 is more active in the context of a heterologous suboptimal splice site than of an optimal 3' splice site. ESS3 inhibits splicing by blocking the formation of a functional spliceosome at an early step, since A complexes are not detected in the presence of ESS3. Competitor RNAs containing either ESS2 or ESS3 relieve inhibition of splicing of substrates containing ESS3 or ESS2. This suggests that a common cellular factor(s) may be required for the inhibition of tat mRNAsplicing mediated by ESS2 and ESS3.

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Documento generato il 26/09/20 alle ore 12:01:07