Abstract:
: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.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Hsu SC,Galceran J,Grosschedl Rdoi
10.1128/mcb.18.8.4807subject
Has Abstractpub_date
1998-08-01 00:00:00pages
4807-18issue
8eissn
0270-7306issn
1098-5549journal_volume
18pub_type
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pub_type: 杂志文章
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