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Primer binding site-dependent restriction of murine leukemia virus requires HP1 binding by TRIM28

Daniel Wolf1, Florence Cammas, Régine Losson

  • 1Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University, HHSC 1310, 701 West 168th Street, New York, NY 10032, USA.

Journal of Virology
|February 22, 2008
PubMed

Insights

Tripartite motif-containing protein 28 (TRIM28) is essential for restricting murine leukemia virus (MLV) replication in specific cells. Its interaction with Heterochromatin protein 1 (HP1) is crucial for this antiviral defense mechanism.

Area of Science:

  • Molecular Biology
  • Virology
  • Epigenetics

Background:

  • Tripartite motif-containing protein 28 (TRIM28) acts as a transcriptional corepressor.
  • TRIM28 mediates the restriction of murine leukemia virus (MLV) replication in embryonic stem and carcinoma cells via primer binding site (PBS) dependence.
  • This restriction involves transcriptional silencing of the provirus and recruitment of Heterochromatin protein 1 (HP1) to silenced genetic loci.

Purpose of the Study:

  • To investigate the role of the TRIM28-HP1 interaction in PBS-dependent MLV restriction.
  • To determine if HP1 recruitment by TRIM28 is essential for MLV transcriptional silencing.

Main Methods:

  • Utilized a cell line engineered with a point mutation in the HP1 binding domain of TRIM28.
  • Assessed MLV replication and proviral silencing in the mutant cell line.
  • Analyzed TRIM28-HP1 interaction dynamics.

Main Results:

  • The point mutation in the TRIM28 HP1 binding domain abolished the PBS-dependent restriction of MLV.
  • TRIM28-mediated recruitment of HP1 to silenced loci was demonstrated to be essential for MLV restriction.
  • The interaction between TRIM28 and HP1 is critical for the antiviral activity in F9 EC cells.

Conclusions:

  • The interaction between TRIM28 and HP1 is indispensable for the primer binding site-dependent restriction of MLV.
  • TRIM28's ability to recruit HP1 is a key mechanism for achieving MLV transcriptional silencing and antiviral defense in embryonic carcinoma cells.

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