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Molecular and Cellular Biology, December 2004, p. 10256-10262, Vol. 24, No. 23
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.23.10256-10262.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

B-Cell Translocation Gene 2 (Btg2) Regulates Vertebral Patterning by Modulating Bone Morphogenetic Protein/Smad Signaling

Sean Park,1,2 Young Jae Lee,1 Ho-Jae Lee,3 Tsugio Seki,1 Kwon-Ho Hong,1 Joonil Park,1 Hideyuki Beppu,4 In Kyung Lim,5 Ji-Won Yoon,2 En Li,4 Seong-Jin Kim,3 and S. Paul Oh1*

Department of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville, Florida,1 Department of Microbiology and Immunology, Center for Immunologic Research, Bligh Cancer Research Laboratories, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois,2 Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland,3 Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts,4 Department of Biochemistry and Molecular Biology, School of Medicine, Ajou University, Suwon, South Korea5

Received 29 April 2004/ Returned for modification 13 June 2004/ Accepted 1 September 2004

Btg2 is a primary p53 transcriptional target gene which may function as a coactivator-corepressor and/or an adaptor molecule that modulates the activities of its interacting proteins. We have generated Btg2-null mice to elucidate the in vivo function of Btg2. Btg2-null mice are viable and fertile but exhibit posterior homeotic transformations of the axial vertebrae in a dose-dependent manner. Consistent with its role in vertebral patterning, Btg2 is expressed in the presomitic mesoderm, tail bud, and somites during somitogenesis. We further provide biochemical evidence that Btg2 interacts with bone morphogenetic protein (BMP)-activated Smads and enhances the transcriptional activity of BMP signaling. In view of the genetic evidence that reduced BMP signaling causes posteriorization of the vertebral pattern, we propose that the observed vertebral phenotype in Btg2-null mice is due to attenuated BMP signaling.

* Corresponding author. Mailing address: Department of Physiology and Functional Genomics, University of Florida, 1600 SW Archer Rd., Room D533d, Gainesville, FL 32610. Phone: (352) 392-8197. Fax: (352) 846-0270. E-mail: ohp{at}phys.med.ufl.edu.

Molecular and Cellular Biology, December 2004, p. 10256-10262, Vol. 24, No. 23
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.23.10256-10262.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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