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Extracellular addition of a domain of HIV-1 Vpr containing the amino acid sequence motif H(S/F)RIG causes cell membrane permeabilization and death.
Macreadie, I G; Arunagiri, C K; Hewish, D R; White, J F; Azad, A A.
Afiliación
  • Macreadie IG; Biomolecular Research Institute, Division of Biomolecular Engineering, Parkville, Victoria, Australia. ianm@mel.dbe.csiro.au
Mol Microbiol ; 19(6): 1185-92, 1996 Mar.
Article en En | MEDLINE | ID: mdl-8730861
Vpr is a virion-associated protein of human immunodeficiency virus type 1 (HIV-1) whose function in acquired immune deficiency syndrome (AIDS) has been uncertain. We previously employed yeast as a model to examine the effects of Vpr on basic cellular functions; intracellular Vpr was shown to cause cell-growth arrest and structural defects, and these effects were caused by a region of Vpr containing the sequence HFRIGCRHSRIG. Here we show that peptides containing the H(S/F)RIG amino acid sequence motif cause death when added externally to a variety of yeast including Saccharomyces cerevisiae, Kluyveromyces lactis, Candida glabrata, Candida albicans and Schizosaccharomyces pombe. Such peptides rapidly entered the cell from the time of addition, resulting in cell death. Elevated levels of ions, particularly magnesium and calcium ions, abrogated the cytotoxic effect by preventing the Vpr peptides from entering the cells. Extracellular Vpr found in the serum, or breakdown products of extracellular Vpr, may have similar effects to the Vpr peptides described here and could explain the death of uninfected bystander cells during AIDS.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: VIH-1 / Productos del Gen vpr Tipo de estudio: Etiology_studies Límite: Humans Idioma: En Revista: Mol Microbiol Asunto de la revista: BIOLOGIA MOLECULAR / MICROBIOLOGIA Año: 1996 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Reino Unido
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: VIH-1 / Productos del Gen vpr Tipo de estudio: Etiology_studies Límite: Humans Idioma: En Revista: Mol Microbiol Asunto de la revista: BIOLOGIA MOLECULAR / MICROBIOLOGIA Año: 1996 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Reino Unido