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Published on December 1, 2006; 10.1104/pp.106.090878


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Received October 5, 2006
Accepted November 21, 2006

Cell Death Suppressor, Arabidopsis BI-1, Is Associated with Calmodulin-binding and Ion Homeostasis

Yuri Ihara-Ohori , Minoru Nagano , Shoshi Muto , Hirofumi Uchimiya , and Maki Kawai-Yamada *

Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan
Nagoya University Bioscience Center, Nagoya University, Chikusa, Nagoya 464-8601, Japan
Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan; Iwate Biotechnology Research Center, Kitakami, Iwate 024-0003, Japan
Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan; Japan Science and Technology Agency (JST), CREST, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan

* Corresponding author; email: mkawai{at}iam.u-tokyo.ac.jp.

Cell death suppressor Bax inhibitor-1 (BI-1), an endoplasmic reticulum (ER) membrane protein, exists in a wide range of organisms. The split-ubiquitin system, overlay assay and the bimolecular fluorescence complementation (BiFC) analysis demonstrated that Arabidopsis BI-1 (AtBI-1) interacted with calmodulin (CaM) in yeast and in plant cells. Furthermore, AtBI-1 failed to rescue yeast mutants lacking Ca2+-ATPase (Pmr1 or Spf1) from Bax-induced cell death. Pmr1 and Spf1, p-type ATPases localized at inner membrane, are believed to be involved in transmembrane movement of calcium ion in yeast. Thus, the presence of intact Ca2+-ATPases was essential for AtBI-1-mediated cell death suppression in yeast. To investigate the effect of AtBI-1 on calcium homeostasis, we evaluated sensitivity against cyclopiazonic acid (CPA), an inhibitor of SERCA-type Ca2+ ATPases, in AtBI-1 overexpressing or knock-down transgenic Arabidopsis plants. These plants demonstrated altered CPA or ion stress sensitivities. Furthermore, AtBI-1 overexpressing cells demonstrated attenuated rise in cytosolic calcium following CPA- or H2O2- treatment, suggesting that AtBI-1 affects ion homeostasis in plant cell death regulation.




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