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J. Biol. Chem., Vol. 280, Issue 47, 39468-39473, November 25, 2005
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From the
Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan, the
Laboratory for DNA Data Analysis, Center for Information Biology, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan, the ¶Institute of Genetic Engineering, Kyungpook National University, Taegu 702-701, Korea, the ||Department of Integrate Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba 277-8562, Japan, and the **Iwate Biotechnology Research Center, Kitakami, Iwate 024-0003, Japan
Overexpression of the mammalian proapoptotic protein Bax induces cell death in plant and yeast cells. The Bax inihibitor-1 (BI-1) gene rescues yeast and plant from Bax-mediated lethality. Using the Arabidopsis BI-1 (AtBI-1) gene controlled by the GAL1 promoter as a cell death suppressor in yeast, Cdf1 (cell growth defect factor-1) was isolated from Arabidopsis cDNA library. Overexpression of Cdf1 caused cell death in yeast, whereas such an effect was suppressed by co-expression of AtBI-1. The Cdf1 protein fused with a green fluorescent protein was localized in the mitochondria and resulted in the loss of mitochondrial membrane potential in yeast. The Bax-resistant mutant BRM1 demonstrated tolerance against Cdf1-mediated lethality, whereas the
atp4 strain was sensitive to Cdf1. Our results suggest that Cdf1 and Bax cause mitochondria-mediated yeast lethality through partially overlapped pathways.
Received for publication, September 1, 2005
* This work was supported by a Grant-in-aid for Scientific Research on Priority Areas 17051006 from the Ministry of Education, Culture, Sports, Science and Technology of Japan and grants from the Ministry of Agriculture, Forestry, and Fisheries of Japan and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 To whom correspondence should be addressed. Tel.: 81-3-5841-7845; Fax: 81-3-5841-8466; E-mail: mkawai{at}iam.u-tokyo.ac.jp.
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