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J. Biol. Chem., Vol. 283, Issue 2, 977-987, January 11, 2008

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-Catenin-induced Dendritic Morphogenesis

AN ESSENTIAL ROLE OF p190RhoGEF INTERACTION THROUGH AKT1-MEDIATED PHOSPHORYLATION^*

Hangun Kim¹, Jeong-Ran Han¹, Jaejun Park, Minsoo Oh, Sarah E. James^¶, Sunghoe Chang, Qun Lu^¶, Kwang Youl Lee, Hyunkyoung Ki, Woo-Joo Song^||, and Kwonseop Kim²

From the College of Pharmacy and Research Institute of Drug Development, Chonnam National University, Gwangju 500-757, Korea, the Department of Life Science, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea, the ^¶Department of Anatomy and Cell Biology, The Brody School of Medicine, East Carolina University, Greenville, North Carolina 27834, and the ^||Graduate Program in Neuroscience and Institute for Brain Science and Technology, Inje University, Daejeon 614-735, Korea

-Catenin was first identified through its interaction with Presenilin-1 and has been implicated in the regulation of dendrogenesis and cognitive function. However, the molecular mechanisms by which -catenin promotes dendritic morphogenesis were unclear. In this study, we demonstrated -catenin interaction with p190RhoGEF, and the importance of Akt1-mediated phosphorylation at Thr-454 residue of -catenin in this interaction. We have also found that -catenin overexpression decreased the binding between p190RhoGEF and RhoA, and significantly lowered the levels of GTP-RhoA but not those of GTP-Rac1 and -Cdc42. -Catenin T454A, a defective form in p190RhoGEF binding, did not decrease the binding between p190RhoGEF and RhoA. -Catenin T454A also did not lower GTP-RhoA levels and failed to induce dendrite-like process formation in NIH 3T3 fibroblasts. Furthermore, -catenin T454A significantly reduced the length and number of mature mushroom shaped spines in primary hippocampal neurons. These results highlight signaling events in the regulation of -catenin-induced dendrogenesis and spine morphogenesis.

Received for publication, August 27, 2007 , and in revised form, November 5, 2007.

^* This study was supported in part by Grant A040042 of the Korea Health 21 R&D Project (to K. K.), Ministry of Health & Welfare, Republic of Korea, and by Grant M103KV010009-06K2201-00910 (to S. C.) from the Brain Research Center of 21^st Century Frontier Research Program (funded by the Ministry of Science and Technology, Republic of Korea and US National Institutes of Health Grants AG026630 (to Q. L.) and CA111891 (to Q. L.). 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.

The on-line version of this article (available at http://www.jbc.org) contains Supplemental Figs. S1-S3.

¹ These authors contributed equally to this study.

² To whom correspondence should be addressed: College of Pharmacy, Chonnam National University, Bldg. 1-211, 300 Yongbong-dong, Gwangju 500-757, Korea. Tel.: 82-62-530-2937; Fax: 82-62-530-2949; E-mail: koskim{at}chonnam.ac.kr.

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