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Molecular and Cellular Biology, March 2008, p. 2059-2065, Vol. 28, No. 6
0270-7306/08/$08.00+0     doi:10.1128/MCB.01362-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

macroH2A1-Dependent Silencing of Endogenous Murine Leukemia Viruses{triangledown} ,{dagger}

Lakshmi N. Changolkar, Geetika Singh, and John R. Pehrson*

Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Received 28 July 2007/ Returned for modification 25 September 2007/ Accepted 27 December 2007

We show that macroH2A1 histone variants are important for repressing the expression of endogenous murine leukemia viruses (MLVs) in mouse liver. Intact MLV proviruses and proviruses with deletions in env were nearly silent in normal mouse liver and showed substantial derepression in macroH2A1 knockout liver. In contrast, MLV proviruses with a deletion in the 5' end of pro-pol were expressed in normal liver and showed relatively low levels of derepression in knockout liver. macroH2A1 nucleosomes were enriched on endogenous MLVs, with the highest enrichment occurring on the 5' end of pro-pol. The absence of macroH2A1 also led to a localized loss of DNA methylation on the 5' ends of MLV proviruses. These results demonstrate that macroH2A1 histones have a significant role in silencing endogenous MLVs in vivo and suggest that specific internal MLV sequences are targeted by a macroH2A1-dependent silencing mechanism.

* Corresponding author. Mailing address: Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104. Phone: (215) 898-0454. Fax: (215) 573-5189. E-mail: pehrson{at}vet.upenn.edu

{triangledown} Published ahead of print on 14 January 2008.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, March 2008, p. 2059-2065, Vol. 28, No. 6
0270-7306/08/$08.00+0     doi:10.1128/MCB.01362-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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