HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Asoh, S. Articles by Ohta, S. Search for Related Content PubMed PubMed Citation Articles by Asoh, S. Articles by Ohta, S. Social Bookmarking                      What's this?

J Biol Chem, Vol. 273, Issue 18, 11384-11391, May 1, 1998

A Trace Amount of the Human Pro-apoptotic Factor Bax Induces Bacterial Death Accompanied by Damage of DNA

From the Department of Biochemistry and Cell Biology, Institute of Gerontology, Nippon Medical School, 1-396, Kosugi-cho, Nakahara-ku, Kawasaki-city, Kanagawa 211-0063, Japan

An amount of human pro-apoptotic Bax as low as 0.01% of total protein was sufficient to cause cell death in Escherichia coli. The bacterial cell death was examined using a viable bacteria-specific fluorescence indicator system and loss of colony formation ability. Co-expression of anti-apoptotic Bcl-x_L showed a modest inhibitory effect on the cell death caused by Bax. The trace amount of Bax elongated E. coli and accumulated monounsaturated fatty acids, suggesting an unusual metabolism of redox in the host. In fact, an increase of KCN-dependent O₂ consumption accompanied the expression of Bax. At the same time, a fluorescent pH indicator showed the apparent accumulation of protons outside the cell, suggesting that the membrane is intact. Bax increased the level of superoxide anion as measured by the expression of superoxide-dependent promoter. Nicked DNA was significantly generated, and the frequency of mutations resistant to rifampicin was increased by 30-fold, depending upon the expression of Bax. It is proposed that trace amounts of Bax increase oxygen consumption, triggering generation of superoxide, which affects DNA, leading to bacterial death.

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				D. J. Adams, L. van der Weyden, A. Mayeda, S. Stamm, B. J. Morris, and J. E.J. Rasko ZNF265--a novel spliceosomal protein able to induce alternative splicing J. Cell Biol., July 9, 2001; 154(1): 25 - 32. [Abstract] [Full Text] [PDF]

				S. C. Kampranis, R. Damianova, M. Atallah, G. Toby, G. Kondi, P. N. Tsichlis, and A. M. Makris A Novel Plant Glutathione S-Transferase/Peroxidase Suppresses Bax Lethality in Yeast J. Biol. Chem., September 15, 2000; 275(38): 29207 - 29216. [Abstract] [Full Text] [PDF]