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Recruitment of chromatin-modifying enzymes by CTIP2 promotes HIV-1 transcriptional silencing.

Following entry and reverse transcription, the HIV-1 genome is integrated into the host genome. In contrast to productively infected cells, latently infected cells frequently harbor HIV-1 genomes integrated in heterochromatic structures, allowing persistence of transcriptionally silent proviruses. Microglial cells are the main HIV-1 target cells in the central nervous system and constitute an important reservoir for viral pathogenesis. In the present work, we show that, in microglial cells, the co-repressor COUP-TF interacting protein 2 (CTIP2) recruits a multienzymatic chromatin-modifying complex and establishes a heterochromatic environment at the HIV-1 promoter. We report that CTIP2 recruits histone deacetylase (HDAC)1 and HDAC2 to promote local histone H3 deacetylation at the HIV-1 promoter region. In addition, DNA-bound CTIP2 also associates with the histone methyltransferase SUV39H1, which increases local histone H3 lysine 9 methylation. This allows concomitant recruitment of HP1 proteins to the viral promoter and formation of local heterochromatin, leading to HIV-1 silencing. Altogether, our findings uncover new therapeutic opportunities for purging latent HIV-1 viruses from their cellular reservoirs.

Pubmed ID: 17245431


  • Marban C
  • Suzanne S
  • Dequiedt F
  • de Walque S
  • Redel L
  • Van Lint C
  • Aunis D
  • Rohr O


The EMBO journal

Publication Data

January 24, 2007

Associated Grants


Mesh Terms

  • Cells, Cultured
  • Chromatin
  • DNA-Binding Proteins
  • Gene Silencing
  • HIV-1
  • Histone Deacetylase 1
  • Histone Deacetylase 2
  • Histone Deacetylases
  • Histone-Lysine N-Methyltransferase
  • Histones
  • Humans
  • Methyltransferases
  • Models, Biological
  • Promoter Regions, Genetic
  • Protein Binding
  • Protein Methyltransferases
  • Repressor Proteins
  • Transcription, Genetic
  • Tumor Suppressor Proteins
  • Virus Replication