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Journal of Virology, November 2002, p. 11283-11290, Vol. 76, No. 22
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.22.11283-11290.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Requirement of BAX for Efficient Adenovirus-Induced Apoptosis

Elena Lomonosova, T. Subramanian, and G. Chinnadurai*

Institute for Molecular Virology, Saint Louis University School of Medicine, St. Louis, Missouri 63110

Received 12 April 2002/ Accepted 6 August 2002

Infection of human epithelial cells with adenoviruses induces an apoptosis paradigm that is efficiently suppressed by the expression of viral E1B-19K protein, which is a functional homolog of the cellular antiapoptosis protein BCL-2. The mechanisms of adenovirus (Ad)-induced apoptosis appear to involve the cellular BCL-2 family proapoptotic proteins. Recent genetic studies with fibroblasts derived from mutant mouse embryos indicate that a class of the BCL-2 family proapoptotic proteins (designated BH-123 or multidomain proteins) such as BAX and BAK constitutes an essential component of the core apoptosis machinery in animal cells. We have examined the role of BAX in Ad-induced apoptosis in human epithelial cells using two colon cancer cell lines, HCT116Bax (Bax+/-) and HCT116BaxKO (Bax-/-) (L. Zhang, J. Yu, B. H. Park, K. W. Kinzler, and B. Vogelstein, Science 290:989-992, 2000). Infection of Bax+/- cells with an Ad type 2 mutant (dl250) defective in expression of the E1B-19K protein resulted in enhanced cytopathic effect, large plaques on cell monolayers, fragmentation of cellular DNA, and enhanced cell death. These mutant phenotypes were not efficiently expressed in Bax-/- cells, suggesting that BAX is essential for Ad-induced apoptosis. Infection of Bax+/- cells with dl250 induced increased levels of an N-terminally processed form of BAX. Cells infected with the 19K mutant also contained enhanced levels of truncated BAX in membrane-inserted form. Our results suggest that at least a part of the mechanism utilized by E1B-19K to suppress apoptosis during Ad infection may involve modulation of the activities of BAX.

* Corresponding author. Mailing address: Institute for Molecular Virology, Saint Louis University School of Medicine, 3681 Park Ave., St. Louis, MO 63110. Phone: (314) 577-8416. Fax: (314) 577-8406. E-mail: Chinnag{at}slu.edu.

Journal of Virology, November 2002, p. 11283-11290, Vol. 76, No. 22
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.22.11283-11290.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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