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Journal of Virology, December 2002, p. 11809-11818, Vol. 76, No. 23
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.23.11809-11818.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
and William R. Folk*
Department of Biochemistry, University of MissouriColumbia, Columbia, Missouri 65211
Received 13 June 2002/ Accepted 23 August 2002
When tethered in cis to DNA, the transcriptional corepressor mSin3B inhibits polyomavirus (Py) ori-dependent DNA replication in vivo. Histone deacetylases (HDACs) appear not to be involved, since tethering class I and class II HDACs in cis does not inhibit replication and treating the cells with trichostatin A does not specifically relieve inhibition by mSin3B. However, the mSin3B L59P mutation that impairs mSin3B interaction with N-CoR/SMRT abrogates inhibition of replication, suggesting the involvement of N-CoR/SMRT. Py large T antigen interacts with mSin3B, suggesting an HDAC-independent mechanism by which mSin3B inhibits DNA replication.
Present address: Harvard Institute of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215.
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