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EBNA2 and Activated Notch Induce Expression of BATF

Lisa M. Johansen,^1, Christopher D. Deppmann,¹ Kimberly D. Erickson,^2, William F. Coffin III,² Tina M. Thornton,¹ Sean E. Humphrey,¹ Jennifer M. Martin,² and Elizabeth J. Taparowsky^1*

Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392,¹ Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Colorado 80309²

Received 14 June 2002/ Accepted 20 February 2003

The immortalization of human B lymphocytes by Epstein-Barr virus (EBV) requires the virus-encoded transactivator EBNA2 and the products of both viral and cellular genes which serve as EBNA2 targets. In this study, we identified BATF as a cellular gene that is up-regulated dramatically within 24 h following the infection of established and primary human B cells with EBV. The transactivation of BATF is mediated by EBNA2 in a B-cell-specific manner and is duplicated in non-EBV-infected B cells by the expression of mammalian Notch proteins. In contrast to other target genes activated by EBNA2, the BATF gene encodes a member of the AP-1 family of transcription factors that functions as a negative regulator of AP-1 activity and as an antagonist of cell growth. A potential role for BATF in promoting EBV latency is supported by studies in which BATF was shown to negatively impact the expression of a BZLF1 reporter gene and to reduce the frequency of lytic replication in latently infected cells. The identification of BATF as a cellular target of EBV provides important new information on how programs of viral and cellular gene expression may be coordinated to promote viral latency and control lytic-cycle entry.

Present address: CombinatoRx, Inc., Boston, MA 02118.

Present address: Department of Microbiology, University of Colorado Health Sciences Ctr., Denver, CO 80262.

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