Role of RNA structure and protein factors in the control of HIV-1 splicing

Jean-Michel Saliou Cyril Bourgeois 1 L. Ayadi-Ben Mena Delphine Ropers 2, * S. Jacquenet V. Marchand 3 James Stévenin Christiane Branlant
* Auteur correspondant
2 IBIS - Modeling, simulation, measurement, and control of bacterial regulatory networks
LAPM - Laboratoire Adaptation et pathogénie des micro-organismes [Grenoble], Inria Grenoble - Rhône-Alpes, Institut Jean Roget
Abstract : Alternative splicing plays a key role in the production of numerous proteins by complex lentiviruses such as HIV-1. The study of HIV-1 RNA splicing has provided useful information not only about the physiology of the virus, but also about the general mechanisms that regulate mammalian pre-mRNA alternative splicing. Like all retroviruses, a fraction of HIV-1 transcripts remains intact to serve as genomic RNA and to code for Gag and Gag-Pol protein precursors. In addition, splicing is important for controlling the production of some viral proteins, which could otherwise have a negative effect on the infected cell. Here, we summarize how the utilization of HIV-1 splicing sites is limited by the binding of nuclear factors to cis-acting silencer elements, taking into account the role of RNA secondary structure in these mechanisms. We also describe how the poorly efficient HIV-1 acceptor sites are nevertheless activated by serine/arginine-rich proteins. Finally, we discuss how nuclear factors that interact with both the transcription and splicing machineries also participate in the control of HIV-1 RNA splicing.
Liste complète des métadonnées
Contributeur : Gaëlle Rivérieux <>
Soumis le : jeudi 21 février 2013 - 14:32:14
Dernière modification le : mercredi 11 avril 2018 - 01:59:58


  • HAL Id : hal-00793011, version 1



Jean-Michel Saliou, Cyril Bourgeois, L. Ayadi-Ben Mena, Delphine Ropers, S. Jacquenet, et al.. Role of RNA structure and protein factors in the control of HIV-1 splicing. Frontiers in Bioscience, Frontiers in Bioscience, 2009, 14, pp.2714-2729. 〈hal-00793011〉



Consultations de la notice