Mutation of the major 5′ splice site renders a CMV‐driven HIV‐1 proviral clone Tat‐dependent: connections between transcription and splicing

FEBS Letters

Kräusslich, Hans-Georg¹  Bohne, Jens¹ 

[1] Department of Virology, Universität Heidelberg, Im Neuenheimer Feld 324, D-69120 Heidelberg, Germany

关键词: Human immunodeficiency virus;    Transcription;    Splicing;    Cytomegalovirus promoter;    Tat;    HIV;    human immunodeficiency virus;    CMV;    cytomegalovirus;    LTR;    long terminal repeat;    Tat;    transactivator of transcription;    TAR;    transactivation response element;    pol II;    RNA polymerase II;    ss;    splice site;    CTD;    C-terminal domain;   

DOI  :  10.1016/S0014-5793(04)00277-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Efficient transcription from the human immunodeficiency virus type 1 long terminal repeat (HIV-1 LTR) promoter is dependent on the viral transactivator Tat. To generate a Tat-independent proviral plasmid, we replaced the promoter in the HIV-1 LTR with the immediate early promoter of cytomegalovirus. Transfection of this plasmid yielded Tat-independent production of infectious HIV-1. Tat-independent expression was lost, however, when the major 5′ splice site in the HIV-1 genome was mutated and no HIV-1-specific RNA or protein was detected. This defect was restored when a Tat expression plasmid was cotransfected. Our results support recent reports indicating an influence of the recognition of splice sites on efficient transcriptional elongation.

【 授权许可】

Unknown