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Journal of Virology, July 2000, p. 5819-5824, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

The E4-6/7 Protein Functionally Compensates for the Loss of E1A Expression in Adenovirus Infection

Robert J. O'Connordagger and Patrick Hearing*

Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York, Stony Brook, New York 11794

Received 11 October 1999/Accepted 6 April 2000

The E1A gene products are required and sufficient for activation of adenovirus gene expression in cultured cells. The E4-6/7 gene product induces the binding of the cellular transcription factor E2F to the viral E2a promoter region. The induction of E2F binding to the E2a promoter in vitro is directly correlated with transcriptional activation of the E2a promoter in vivo. The E2 region encodes the viral replication proteins, yet adenoviruses lacking E4-6/7 function demonstrate no defective phenotype in infected cells. Here we show that the E4-6/7 protein can functionally compensate for E1A expression in virus infection. In the absence of the E1A gene products, expression of the E4-6/7 protein is sufficient to displace retinoblastoma protein family members from E2Fs, activate expression of early region 2 via induction of E2F DNA binding to the E2a promoter region, and significantly enhance replication of an E1A-defective adenovirus. These results have implications in the regulation of viral gene expression and for the development of recombinant adenovirus vectors.

* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York, Stony Brook, NY 11794. Phone: (631) 632-8813. Fax: (631) 632-8891. E-mail: phearing{at}ms.cc.sunysb.edu.

dagger Present address: Department of Anatomy, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143.

Journal of Virology, July 2000, p. 5819-5824, Vol. 74, No. 13
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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