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J. Biol. Chem., Vol. 279, Issue 27, 28509-28514, July 2, 2004

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Phosphatidylinositol 3-Kinase Signaling Is Involved in Neurogenesis during Xenopus Embryonic Development^*

Ying Peng¶, Bing-Hua Jiang¶||, Pai-Hao Yang, Zongxian Cao||, Xianglin Shi**, Marie C. M. Lin, Ming-Liang He, and Hsiang-fu Kung

From the Department of Neurology, Nanfang Hospital, The First Military Medical University, Guangzhou 510515, China, the Institute of Molecular Biology, The University of Hong Kong, Hong Kong, China, the ^||Mary Babb Randolph Cancer Center, Department of Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, West Virginia 26506, and the ^**Institute for Nutritional Sciences, Chinese Academy of Sciences, 294 Tai Yuan Road, Shanghai 200031, China

Phosphatidylinositol 3-kinase (PI3K) has numerous cellular functions, including cell survival and proliferation. In this study, we demonstrated that the expression of the active form of PI3K induced dorsal differentiation and axis duplication and strongly induced the expression of neural markers. In contrast, the inhibition of PI3K activity by its dominant negative mutant induced the phenotype of losing posterior structures and the expression of ventral markers. Akt is an essential target of PI3K for neurogenesis. The expression of the active form of Akt induced axis duplication and increased the expression of neural markers. Inhibition of the Akt activity abolished the PI3K-induced double heads and axes. This signal transmits through its target, glycogen synthase kinase 3, which is known to mediate Wnt signaling for Xenopus development. These results identify a new function of PI3K/Akt signaling in axis formation and neurogenesis during Xenopus embryonic development and provide a direct link between growth factor-mediated PI3K/Akt signaling and Wnt signaling during embryonic development.

Received for publication, March 1, 2004 , and in revised form, April 26, 2004.

^* This work was supported in part by National Institutes of Health Grant RR16440, American Heart Association Grant 0160166B, American Cancer Society Research Scholar Grant 04-076-01-TBE (to B.-H. J.), and Research Grants Council of the Hong Kong Special Administrative Region, China Grants (HKU 7166/99 M and NSFC/HKU20 (to H.-f. K.) and HKU 7198/01 M (to M. C. M. 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.

^¶ These two authors contributed equally to the manuscript.

To whom correspondence should be addressed: 8/F, Kadoorie Biological Science Bldg., Inst. of Molecular Biology, The University of Hong Kong, Pokfulam Rd., Hong Kong. Tel.: 852-22990750; Fax: 852-28171006; E-mail: hkung{at}hkucc.hku.hk.

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