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| Subject Categories: Cell Cycle |
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| The EMBO Journal
(2002) 21, 6419–6428, doi: 10.1093/emboj/cdf659 |
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| Identification of a MAD2-binding protein, CMT2, and its role in mitosis |
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| Toshiyuki Habu1, 2, Sang Hoon Kim1, 3, Jasminder Weinstein4 and Tomohiro Matsumoto1, 5 |
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1 Department of Radiation Oncology and Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA 2 Present address: Radiation Biology Center, Kyoto University, Yoshida-Konoe cho, Sakyo ku, Kyoto, Japan 3 Present address: Department of Biology, Kyung Hee University, Seoul, 130-701, Republic of Korea 4 Department of Amgen Inc., 5-2-A, One Amgen Center Drive, Thousand Oaks, CA 91320, USA 5 Radiation Biology Center, Kyoto University, Yoshida-Konoe cho, Sakyo ku, Kyoto, Japan To whom correspondence should be addressed Tomohiro Matsumoto, tmatsumo@house.rbc.kyoto-u.ac.jp Received 3 July 2002; Revised 24 September 2002; Accepted 18 October 2002. |
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| Abstract |
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| MAD2 is a key component of the spindle checkpoint that delays the onset of anaphase until all the kinetochores are attached to the spindle. It binds to human p55CDC and prevents it from promoting destruction of an anaphase inhibitor, securin. Here we report the characterization of a novel MAD2-binding protein, CMT2. Upon the completion of spindle attachment, formation of the CMT2−MAD2 complex coincides with dissociation of the p55CDC−MAD2 complex. Overexpression of CMT2 in cells arrested by the spindle checkpoint causes premature destruction of securin and allows exit from mitosis without chromosome segregation. Depletion of CMT2 induces cell death following a transient delay in the onset of anaphase. These results indicate that CMT2 interacts with the spindle checkpoint and coordinates cell cycle events in late mitosis. |
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| Keywords: CMT2, MAD2, mitosis, spindle checkpoint |
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