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Mol Cell Biol, August 1998, p. 4807-4818, Vol. 18, No. 8
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Modulation of Transcriptional Regulation by LEF-1 in Response to Wnt-1 Signaling and Association with beta -Catenin

Shu-Chi Hsu, Juan Galceran, and Rudolf Grosschedl*

Howard Hughes Medical Institute, Departments of Microbiology and Biochemistry, University of California, San Francisco, California 94143-0414

Received 10 March 1998/Returned for modification 14 April 1998/Accepted 26 May 1998

Wnt signaling is thought to be mediated via interactions between beta -catenin and members of the LEF-1/TCF family of transcription factors. Here we study the mechanism of transcriptional regulation by LEF-1 in response to a Wnt-1 signal under conditions of endogenous beta -catenin in NIH 3T3 cells, and we examine whether association with beta -catenin is obligatory for the function of LEF-1. We find that Wnt-1 signaling confers transcriptional activation potential upon LEF-1 by association with beta -catenin in the nucleus. By mutagenesis, we identified specific residues in LEF-1 important for interaction with beta -catenin, and we delineated two transcriptional activation domains in beta -catenin whose function is augmented in specific association with LEF-1. Finally, we show that a Wnt-1 signal and beta -catenin association are not required for the architectural function of LEF-1 in the regulation of the T-cell receptor alpha  enhancer, which involves association of LEF-1 with a different cofactor, ALY. Thus, LEF-1 can assume diverse regulatory functions by association with different proteins.

* Corresponding author. Mailing address: Howard Hughes Medical Institute, Departments of Microbiology and Biochemistry, University of California, San Francisco, CA 94143-0414. Phone: (415) 476-6954. Fax: (415) 476-8201. E-mail: rgross{at}itsa.ucsf.edu.

Mol Cell Biol, August 1998, p. 4807-4818, Vol. 18, No. 8
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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