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      XTcf-3 transcription factor mediates beta-catenin-induced axis formation in Xenopus embryos.

      Cell
      Amino Acid Sequence, Animals, Base Sequence, Cytoskeletal Proteins, physiology, DNA, Complementary, Embryonic Induction, Gene Expression Regulation, Developmental, HMGB Proteins, Molecular Sequence Data, Morphogenesis, genetics, Mutagenesis, Site-Directed, Restriction Mapping, TCF Transcription Factors, Trans-Activators, Transcription Factor 3, Transcription Factor 7-Like 1 Protein, Transcription Factors, metabolism, Transcription, Genetic, Xenopus, Xenopus Proteins, beta Catenin

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          Abstract

          XTcf-3 is a maternally expressed Xenopus homolog of the mammalian HMG box factors Tcf-1 and Lef-1. The N-terminus of XTcf-3 binds to beta-catenin. Microinjection of XTcf-3 mRNA in embryos results in nuclear translocation of beta-catenin. The beta-catenin-XTcf-3 complex activates transcription in a transient reporter gene assay, while XTcf-3 by itself is silent. N-terminal deletion of XTcf-3 (delta N) abrogates the interaction with beta-catenin, as well as the consequent transcription activation. This dominant-negative delta N mutant suppresses the induction of axis duplication by microinjected beta-catenin. It also suppresses endogenous axis specification upon injection into the dorsal blastomeres of a 4-cell-stage embryo. We propose that signaling by beta-catenin involves complex formation with XTcf-3, followed by nuclear translocation and activation of specific XTcf-3 target genes.

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