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J. Biol. Chem., Vol. 277, Issue 14, 11904-11909, April 5, 2002

This Article Full Text Full Text (PDF) All Versions of this Article: 277/14/11904    most recent M111788200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yoo, J. Articles by Han, M. Y. Search for Related Content PubMed PubMed Citation Articles by Yoo, J. Articles by Han, M. Y.

Activation of Dynamin I Gene Expression by Sp1 and Sp3 Is Required for Neuronal Differentiation of N1E-115 Cells^*

Jiyun Yoo, Moon-Jin Jeong, Byoung-Mog Kwon, Man-Wook Hur^§, Young-Mee Park^¶, and Mi Young Han^**

From the  Cell Biology Laboratory, Korea Research Institute of Bioscience and Biotechnology, Taejon 305-600, Korea, the ^§ Department of Biochemistry and Molecular Biology, BK 21 Project for Medical Sciences, Institute of Genetic Sciences, Yonsei University School of Medicine, Seoul 120-752, Korea, the ^¶ Department of Biology, College of Natural Sciences, Inchon University, Inchon 402-749, Korea, and the  Green Cross Institute of Medical Genetics, Seoul 135-260, Korea

Dynamin I is a key molecule required for the recycling of synaptic vesicles in neurons, and it has been known that dynamin I gene expression is induced during neuronal differentiation. Our previous studies established that neuronal restriction of dynamin I gene expression is controlled by Sp1 and nuclear factor-B-like element-1. Here, using a series of deletion constructs and site-directed mutation, we found that transcription of dynamin I gene during neuronal differentiation of N1E-115 cells is controlled primarily by the Sp1 element located between 13 to 4 bp of the dynamin I promoter. Gel shift analysis demonstrated that in addition to Sp1, Sp3 could interact with this Sp1 element. The requirement for Sp family transcription factors in dynamin I gene expression was confirmed by using mithramycin, an inhibitor of Sp1/Sp3 binding. Mithramycin repressed dynamin I gene expression and resulted in blocking of neuronal differentiation of N1E-115 cells. The localization of the dynamin I protein was also restricted in the peripheral region of the nucleus by the mithramycin treatment. Thus, all of our results suggest that induction of dynamin I gene expression during N1E-115 cell differentiation is modulated by Sp1/Sp3 interactions with the dynamin I promoter, and its expression is important for neuronal differentiation of the N1E-115 cells.

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