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Genes & Dev. 14 (14): 1734-1740

Copyright © 2000 by Cold Spring Harbor Laboratory Press.

Vol. 14, No. 14, pp. 1734-1740, July 15, 2000

RESEARCH PAPER
Bcl-2 antiapoptotic protein mediates verotoxin II-induced cell death: possible association between Bcl-2 and tissue failure by E. coli O157:H7

Atsushi Suzuki,1,5,6 Hirofumi Doi,2,3,5 Fumiko Matsuzawa,2 Sei-ichi Aikawa,2 Kyoko Takiguchi,2 Hirokazu Kawano,1 Midori Hayashida,1 and Susumu Ohno4

1 Project for the Cell Death Research, Basic Technology Research Laboratory, Daiichi Pharmaceutical Co., Ltd., Tokyo R&D Center, Tokyo 134-8630, Japan; 2 Biological Informatics Section, Fujitsu Laboratories, Ltd., Chiba 261-0023, Japan; 3 Doi Bioasymmetry Project, ERATO, Japan Science and Technology Co., Chiba 263-7112, Japan; 4 Beckman Research Institute of the City of Hope, California 91010-0269, USA

Verotoxin II (VTII: or Shiga-like toxin 2) is a key factor for Escherichia coli O157:H7-induced multiple tissue failure and contains a pentameric sequence (NWGRI) similar to the Bcl-2 homolog domain, BH1. In the current study, we demonstrate that VTII, but not VTI, interacts with Bcl-2 through each BH1 domain pentameric sequence (NWGRI) and that the VTII/Bcl-2 complex is necessary for cell-death induction in target cells. VTII translocates to mitochondria and induces cell death only when target cells are expressing Bcl-2. In addition, interruption of VTII-Bcl-2 complex formation by a pentameric BH1 synthetic peptide suppresses VTII-induced cell death. In the present article, we propose that Bcl-2 mediates VTII-induced target cell death by the interaction with each pentameric sequence of BH1 domain.

[Key Words: Bcl-2; Escherichia coli O157:H7-derived verotoxin II; cell death; multiple tissue failure]


5 These authors are equally contributed to this study.

6 Corresponding author.


GENES & DEVELOPMENT 14:1734-1740 © 2000 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/00 $5.00

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