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Yeast perspectives on HIV-1 VPR.

Y Zhao1, R T Elder

  • 1Children's Memorial Institute for Education and Research, Northwestern University Medical School, 2430 N Halsted Street, MB218, Chicago, Illinois 60614, USA.

Frontiers in Bioscience : a Journal and Virtual Library
|December 5, 2000
PubMed
Summary

HIV-1 viral protein R (Vpr) induces cell cycle arrest and apoptosis by interacting with conserved yeast processes. Studies in yeast reveal Vpr

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Area of Science:

  • * Virology
  • * Molecular Biology
  • * Cell Biology

Background:

  • * HIV-1 viral protein R (Vpr) is implicated in viral pathogenesis.
  • * Vpr functions are linked to viral activation, immune suppression, and CD4+ T-cell depletion, hallmarks of AIDS.
  • * Vpr exhibits diverse in vitro activities, including nuclear transport, cell cycle G2 arrest, and cell death, in both mammalian and yeast cells.

Purpose of the Study:

  • * To investigate the conserved cellular processes Vpr interacts with using yeast models.
  • * To elucidate the mechanisms behind Vpr-induced G2 arrest and cell death.
  • * To understand Vpr's role in nuclear transport and its structural requirements.

Main Methods:

  • * Studies utilizing fission yeast (Schizosaccharomyces pombe) and budding yeast (Saccharomyces cerevisiae).
  • * Analysis of Vpr's interaction with protein phosphatase 2A in G2 arrest.
  • * Investigation of Vpr binding to importin ? for nuclear transport.
  • * Examination of Vpr's effects on mitochondrial membrane permeability.
  • * Mutational analysis of key amino acid residues in Vpr.

Main Results:

  • * Vpr induces G2 arrest via inhibitory phosphorylation of cyclin-dependent kinase, involving protein phosphatase 2A.
  • * Vpr facilitates nuclear transport of the pre-integration complex by binding importin ?.
  • * Vpr induces apoptosis through direct mitochondrial membrane permeabilization and via mitochondrial-independent pathways.
  • * Vpr-induced G2 arrest and cell death are independent functions.
  • * Amino acid residues at positions 29, 33, and 71 are crucial for Vpr structure.

Conclusions:

  • * Yeast serves as a valuable model for studying conserved Vpr activities.
  • * Vpr utilizes highly conserved cellular pathways to induce G2 arrest and cell death.
  • * Understanding Vpr's mechanisms in yeast provides insights into HIV-1 pathogenesis.
  • * Key Vpr residues are essential for its structural integrity and function.

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