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Molecular and Cellular Biology, January 2001, p. 562-574, Vol. 21, No. 2
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.2.562-574.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Identification of a Mouse Homolog of the Human BTEB2 Transcription Factor as a beta -Catenin-Independent Wnt-1-Responsive Gene

Lisa Taneyhill Ziemer,1 Diane Pennica,2 and Arnold J. Levine3,*

Department of Molecular Biology, Princeton University, Princeton, New Jersey 085441; Molecular Oncology Department, Genentech, Inc., South San Francisco, California 940802; and The Rockefeller University, New York, New York 100213

Received 18 May 2000/Returned for modification 27 June 2000/Accepted 28 September 2000

The Wnt/Wg signaling pathway functions during development to regulate cell fate determination and patterning in various organisms. Two pathways are reported to lie downstream of Wnt signaling in vertebrates. The canonical pathway relies on the activation of target genes through the beta -catenin-Lef/TCF complex, while the noncanonical pathway employs the activation of protein kinase C (PKC) and increases in intracellular calcium to induce target gene expression. cDNA subtractive hybridization between a cell line that overexpresses Wnt-1 (C57MG/Wnt-1) and the parental cell line (C57MG) was performed to identify downstream target genes of Wnt-1 signaling. Among the putative Wnt-1 target genes, we have identified a mouse homolog of the gene encoding human transcription factor basic transcription element binding protein 2 (mBTEB2). The mBTEB2 transcript is found at high levels in mammary tissue taken from a transgenic mouse overexpressing Wnt-1 (both tissue prior to active proliferation and tumor tissue) but is barely detectable in wild-type mouse mammary glands. The regulation of mBTEB2 by Wnt-1 signaling in tissue culture occurs through a beta -catenin-Lef/TCF-independent mechanism, as it is instead partially regulated by PKC. The Wnt-1-induced, PKC-dependent activation of mouse BTEB2 in C57MG cells, as well as the ability of Wnt-1 to stabilize beta -catenin in these cells, is consistent with the hypothesis that both the noncanonical and canonical Wnt pathways are activated concomitantly in the same cell. These results suggest that mBTEB2 is a biologically relevant target of Wnt-1 signaling that is activated through a beta -catenin-independent, PKC-sensitive pathway in response to Wnt-1.

* Corresponding author. Mailing address: The Rockefeller University, 1230 York Rd., New York, NY 10021. Phone: (212) 327-8080. Fax: (212) 327-8900. E-mail: alevine{at}rockvax.rockefeller.edu.

Molecular and Cellular Biology, January 2001, p. 562-574, Vol. 21, No. 2
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.2.562-574.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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