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LSD1 cooperates with CTIP2 to promote HIV-1 transcriptional silencing

Valentin Le Douce1, Laurence Colin, Laetitia Redel

  • 1University of Strasbourg, EA4438, Institute of parasitology, Strasbourg, France.

Nucleic Acids Research
|November 10, 2011
PubMed

Insights

The histone demethylase LSD1 and cofactor CTIP2 repress HIV-1 transcription in the central nervous system (CNS). This epigenetic regulation involves specific histone marks, impacting viral reservoirs.

Area of Science:

  • Neurovirology
  • Epigenetics
  • Molecular Biology

Background:

  • Microglial cells are primary targets for HIV-1 in the CNS, forming latent viral reservoirs.
  • The chromatin structure of integrated proviruses is crucial for establishing and maintaining these reservoirs.
  • The cellular cofactor CTIP2 was previously shown to induce heterochromatin and silence HIV-1 by recruiting histone-modifying enzymes.

Purpose of the Study:

  • To investigate the role of the histone demethylase LSD1 in regulating HIV-1 transcription and viral expression.
  • To elucidate the synergistic interaction between LSD1, CTIP2, and HIV-1 gene silencing.
  • To identify the specific epigenetic marks and protein interactions involved in LSD1-mediated repression.

Main Methods:

  • Chromatin immunoprecipitation (ChIP) assays to detect histone modifications (H3K4me3, H3K9me3) at the HIV-1 promoter.
  • Analysis of HIV-1 transcription and viral expression levels.
  • Investigating the recruitment of LSD1 and hSET1 to the viral promoter.

Main Results:

  • LSD1 represses HIV-1 transcription and viral expression synergistically with CTIP2.
  • LSD1 recruitment to the HIV-1 promoter is associated with both H3K4me3 and H3K9me3 epigenetic marks.
  • LSD1-induced H3K4 trimethylation correlates with the recruitment of hSET1 to the integrated provirus.

Conclusions:

  • LSD1 is a key epigenetic repressor of HIV-1 in microglial cells.
  • The interplay between LSD1, CTIP2, and specific histone modifications regulates HIV-1 latency.
  • Targeting LSD1 may offer a novel strategy for controlling HIV-1 reservoirs in the CNS.

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