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Journal of Virology, May 2008, p. 4675-4679, Vol. 82, No. 9
0022-538X/08/$08.00+0 doi:10.1128/JVI.02445-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
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Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University, College of Physicians and Surgeons, New York, New York 10032,1 Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP/Collège de France, BP10142, 67404 Illkirch-Cedex, France2
Received 13 November 2007/ Accepted 9 February 2008
TRIM28 is a transcriptional corepressor which is required for primer binding site (PBS)-dependent restriction of murine leukemia virus (MLV) replication in embryonic stem and embryonic carcinoma (EC) cells. PBS-dependent restriction of MLV leads to transcriptional silencing of the integrated provirus and has been shown to correlate with TRIM28-mediated recruitment of HP1 to the silenced loci. Here we show, using a cell line with a point mutation in the HP1 binding domain of TRIM28, that interaction with HP1 is absolutely required for the PBS-dependent restriction of MLV in the F9 EC cell line.
Published ahead of print on 20 February 2008.
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