Evolutionary Diversification of Vertebrate TCF/LEF Structure, Function, and Regulation

Stefan Hoppler*, Marian L. Waterman

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Citations (Scopus)

Abstract

As a general rule, most genome duplications tend to be lost, and indeed, the complete complement of Wnt signaling components in vertebrates is not four times larger than in invertebrates. The most notable exception, and the most relevant to this chapter, is the TCF/LEF family of DNA-binding factors. Vertebrate and invertebrate TCF/LEF genes share inherited or2uctures and functions. DNA-associated TCF/LEF proteins mediate transcriptional activation when they are bound by nuclear β-catenin, which links to transcriptional coactivators, or they mediate transcriptional repression when bound by transcriptional corepressors. Differential expression of the four vertebrate TCF/LEF genes allows them to be associated with the development of specific tissues, organs, and also diseases; and it provides additional mechanisms for regulating context-specific responses to Wnt signaling. It is interesting to note that the extent of alternative splicing and the degree of similarity to invertebrate orthologs differs among the members of the vertebrate TCF/LEF gene family.

Original languageEnglish
Title of host publicationWnt Signaling in Development and Disease
Subtitle of host publicationMolecular Mechanisms and Biological Functions
PublisherWiley-Blackwell
Pages225-237
Number of pages13
ISBN (Electronic)9781118444122
ISBN (Print)9781118444160
DOIs
Publication statusPublished - 5 May 2014

    Fingerprint

Keywords

  • Differential transcriptional regulation
  • LEF proteins
  • TCF proteins
  • Vertebrates
  • Wnt signaling

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Hoppler, S., & Waterman, M. L. (2014). Evolutionary Diversification of Vertebrate TCF/LEF Structure, Function, and Regulation. In Wnt Signaling in Development and Disease: Molecular Mechanisms and Biological Functions (pp. 225-237). [17] Wiley-Blackwell . https://doi.org/10.1002/9781118444122.ch17