Activation of the ATR-mediated DNA damage response by the HIV-1 viral protein R

J Biol Chem. 2003 Jul 11;278(28):25879-86. doi: 10.1074/jbc.M303948200. Epub 2003 May 8.

Abstract

DNA damage is a universal inducer of cell cycle arrest at the G2 phase. Infection by the human immunodeficiency virus type 1 (HIV-1) also blocks cellular proliferation at the G2 phase. The HIV-1 accessory gene vpr encodes a conserved 96-amino acid protein (Vpr) that is necessary and sufficient for the HIV-1-induced block of cellular proliferation. In the present study, we examined a recently identified DNA damage-signaling protein, the ATM- and Rad3-related protein, ATR, for its potential role in the induction of G2 arrest by Vpr. We show that inhibition of ATR by pharmacological inhibitors, by expression of the dominant-negative form of ATR, or by RNA interference inhibits Vpr-induced cell cycle arrest. As with DNA damage, activation of ATR by Vpr results in phosphorylation of Chk1. This study provides conclusive evidence of activation of the ATR-initiated DNA damage-signaling pathway by a viral gene product. These observations are important toward understanding how HIV infection promotes cell cycle disruption, cell death, and ultimately, CD4+ lymphocyte depletion.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents, Phytogenic / pharmacology
  • Ataxia Telangiectasia Mutated Proteins
  • CD4-Positive T-Lymphocytes / virology
  • Caffeine / pharmacology
  • Cell Cycle
  • Cell Cycle Proteins / metabolism*
  • Cell Division
  • Cell Line, Transformed
  • Chromones / pharmacology
  • DNA Damage*
  • Doxorubicin / pharmacology
  • Enzyme Inhibitors / pharmacology
  • G2 Phase
  • Gene Products, vpr / metabolism*
  • Genes, Dominant
  • Genetic Vectors
  • HIV Infections / virology
  • HeLa Cells
  • Humans
  • Immunoblotting
  • Luciferases / metabolism
  • Morpholines / pharmacology
  • Paclitaxel / pharmacology
  • Phosphorylation
  • Plasmids / metabolism
  • Protein Serine-Threonine Kinases*
  • RNA Interference
  • Signal Transduction
  • Transfection
  • vpr Gene Products, Human Immunodeficiency Virus

Substances

  • Antineoplastic Agents
  • Antineoplastic Agents, Phytogenic
  • Cell Cycle Proteins
  • Chromones
  • Enzyme Inhibitors
  • Gene Products, vpr
  • Morpholines
  • vpr Gene Products, Human Immunodeficiency Virus
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Caffeine
  • Doxorubicin
  • Luciferases
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein Serine-Threonine Kinases
  • Paclitaxel