p120ctn binds to the cytoplasmic domain of cadherins but its role is poorly understood. Colo 205 cells grow as dispersed cells despite their normal expression of E-cadherin and catenins. However, in these cells we can induce typical E-cadherin–dependent aggregation by treatment with staurosporine or trypsin. These treatments concomitantly induce an electrophoretic mobility shift of p120ctn to a faster position. To investigate whether p120ctn plays a role in this cadherin reactivation process, we transfected Colo 205 cells with a series of p120ctn deletion constructs. Notably, expression of NH2-terminally deleted p120ctn induced aggregation. Similar effects were observed when these constructs were introduced into HT-29 cells. When a mutant N-cadherin lacking the p120ctn-binding site was introduced into Colo 205 cells, this molecule also induced cell aggregation, indicating that cadherins can function normally if they do not bind to p120ctn. These findings suggest that in Colo 205 cells, a signaling mechanism exists to modify a biochemical state of p120ctn and the modified p120ctn blocks the cadherin system. The NH2 terminus–deleted p120ctn appears to compete with the endogenous p120ctn to abolish the adhesion-blocking action.
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3 May 1999
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May 03 1999
p120ctn Acts as an Inhibitory Regulator of Cadherin Function in Colon Carcinoma Cells
Shinya Aono,
Shinya Aono
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
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Shinichi Nakagawa,
Shinichi Nakagawa
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
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Albert B. Reynolds,
Albert B. Reynolds
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
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Masatoshi Takeichi
Masatoshi Takeichi
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
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Shinya Aono
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
Shinichi Nakagawa
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
Albert B. Reynolds
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
Masatoshi Takeichi
*Department of Biophysics, Faculty of Science, Kyoto University, Kyoto 606-8502, Japan; and ‡Department of Cell Biology, Vanderbilt University, School of Medicine, Nashville, Tennessee 37232-2175
Address correspondence to Masatoshi Takeichi, Department of Biophysics, Faculty of Science, Kyoto University, Kitashirakawa, Sakyo-ku, Kyoto 606-8502, Japan. Tel.: 81-75-753-4196. Fax: 81-75-753-4197. E-mail: [email protected]
Shinichi Nakagawa's current address is Department of Anatomy, Downing Street, University of Cambridge, Cambridge CB2 3DY, United Kingdom.
Received:
February 05 1999
Revision Received:
March 23 1999
Online ISSN: 1540-8140
Print ISSN: 0021-9525
1999
J Cell Biol (1999) 145 (3): 551–562.
Article history
Received:
February 05 1999
Revision Received:
March 23 1999
Citation
Shinya Aono, Shinichi Nakagawa, Albert B. Reynolds, Masatoshi Takeichi; p120ctn Acts as an Inhibitory Regulator of Cadherin Function in Colon Carcinoma Cells . J Cell Biol 3 May 1999; 145 (3): 551–562. doi: https://doi.org/10.1083/jcb.145.3.551
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