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Journal of Virology, November 2001, p. 10383-10392, Vol. 75, No. 21
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.21.10383-10392.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

DDB2 Induces Nuclear Accumulation of the Hepatitis B Virus X Protein Independently of Binding to DDB1

Alo Nag,1 Abhishek Datta,1 Kyung Yoo,2 Dibyendu Bhattacharyya,2 Amit Chakrabortty,1 Xinhi Wang,2 Betty L. Slagle,3 Robert H. Costa,2 and Pradip Raychaudhuri1,*

Department of Biochemistry and Molecular Biology1 and Department of Molecular Genetics,2 University of Illinois at Chicago, Chicago, Illinois 60612, and Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 770303

Received 1 May 2001/Accepted 30 July 2001

The hepatitis B virus (HBV) X protein (HBx) is critical for the life cycle of the virus. HBx associates with several host cell proteins including the DDB1 subunit of the damaged-DNA binding protein DDB. Recent studies on the X protein encoded by the woodchuck hepadnavirus have provided correlative evidence indicating that the interaction with DDB1 is important for establishment of infection by the virus. In addition, the interaction with DDB1 has been implicated in the nuclear localization of HBx. Because the DDB2 subunit of DDB is required for the nuclear accumulation of DDB1, we investigated the role of DDB2 in the nuclear accumulation of HBx. Here we show that expression of DDB2 increases the nuclear levels of HBx. Several C-terminal deletion mutants of DDB2 that fail to bind DDB1 are able to associate with HBx, suggesting that DDB2 may associate with HBx independently of binding to DDB1. We also show that DDB2 enhances the nuclear accumulation of HBx independently of binding to DDB1, since a mutant that does not bind DDB1 is able to enhance the nuclear accumulation of HBx. HBV infection is associated with liver pathogenesis. We show that the nuclear levels of DDB1 and DDB2 are tightly regulated in hepatocytes. Studies with regenerating mouse liver indicate that during late G1 phase the nuclear levels of both subunits of DDB are transiently increased, followed by a sharp decrease in S phase. Taken together, these results suggest that DDB1 and DDB2 would participate in the nuclear functions of HBx effectively only during the late-G1 phase of the cell cycle.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Biology (M/C 536), University of Illinois at Chicago, 1819 W. Polk St., Chicago, IL 60612-7334. Phone: (312) 413-0255. Fax: (312) 413-0364. E-mail: Pradip{at}uic.edu.

Journal of Virology, November 2001, p. 10383-10392, Vol. 75, No. 21
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.21.10383-10392.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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