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Molecular and Cellular Biology, December 2000, p. 8783-8792, Vol. 20, No. 23
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Runx2 Is a Common Target of Transforming Growth Factor beta 1 and Bone Morphogenetic Protein 2, and Cooperation between Runx2 and Smad5 Induces Osteoblast-Specific Gene Expression in the Pluripotent Mesenchymal Precursor Cell Line C2C12

Kyeong-Sook Lee,1 Hyun-Jung Kim,2 Qing-Lin Li,1 Xin-Zi Chi,1 Chisato Ueta,3 Toshihisa Komori,3 John M. Wozney,4 Eung-Gook Kim,1 Je-Young Choi,2 Hyun-Mo Ryoo,2 and Suk-Chul Bae1,*

Department of Biochemistry, School of Medicine, and Medical Research Institute, Chungbuk National University, Cheongju 361-763,1 Department of Biochemistry, School of Dentistry, and Medical Research Institute, Kyungpook National University, Taegu,2 Korea; Department of Medicine III, Osaka University Medical School, Osaka 565, Japan3; and Genetics Institute, Inc., Cambridge, Massachusetts4

Received 27 June 2000/Returned for modification 22 August 2000/Accepted 8 September 2000

When C2C12 pluripotent mesenchymal precursor cells are treated with transforming growth factor beta 1 (TGF-beta 1), terminal differentiation into myotubes is blocked. Treatment with bone morphogenetic protein 2 (BMP-2) not only blocks myogenic differentiation of C2C12 cells but also induces osteoblast differentiation. The molecular mechanisms governing the ability of TGF-beta 1 and BMP-2 to both induce ligand-specific responses and inhibit myogenic differentiation are not known. We identified Runx2/PEBP2alpha A/Cbfa1, a global regulator of osteogenesis, as a major TGF-beta 1-responsive element binding protein induced by TGF-beta 1 and BMP-2 in C2C12 cells. Consistent with the observation that Runx2 can be induced by either TGF-beta 1 or BMP-2, the exogenous expression of Runx2 mediated some of the effects of TGF-beta 1 and BMP-2 but not osteoblast-specific gene expression. Runx2 mimicked common effects of TGF-beta 1 and BMP-2 by inducing expression of matrix gene products (for example, collagen and fibronectin), suppressing MyoD expression, and inhibiting myotube formation of C2C12 cells. For osteoblast differentiation, an additional effector, BMP-specific Smad protein, was required. Our results indicate that Runx2 is a major target gene shared by TGF-beta and BMP signaling pathways and that the coordinated action of Runx2 and BMP-activated Smads leads to the induction of osteoblast-specific gene expression in C2C12 cells.

* Corresponding author. Mailing address: Department of Biochemistry, School of Medicine, and Medical Research Institute, Chungbuk National University, Cheongju 361-763, South Korea. Phone: 82-43-261-2842. Fax: 82-43-274-8705. E-mail: scbae{at}med.chungbuk.ac.kr.

Molecular and Cellular Biology, December 2000, p. 8783-8792, Vol. 20, No. 23
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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