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Difference in XTcf-3 dependency accounts for change in response to β-catenin-mediated Wnt signalling inXenopusblastula
Author(s) -
Fiona S. Hamilton,
Grant N. Wheeler,
Stefan Hoppler
Publication year - 2001
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.128.11.2063
Subject(s) - wnt signaling pathway , biology , xenopus , mesoderm , blastula , microbiology and biotechnology , fgf and mesoderm formation , beta catenin , signal transduction , lrp6 , embryogenesis , embryonic stem cell , genetics , embryo , gastrulation , gene
Wnt signalling functions in many tissues and during different stages of animal development to produce very specific responses. In early Xenopus embryos there is a dramatic change in response to Wnt signalling within only a few hours of development. Wnt signalling in very early embryos leads to a dorsalising response, which establishes the endogenous dorsal axis. Only a few hours later in development, almost the opposite happens: Xwnt-8 functions to pattern the embryonic mesoderm by promoting ventral and lateral mesoderm. The specificity of the response could conceivably be carried out by differential use of different signal transduction pathways, many of which have recently been described. We have found, however, that this dramatic shift in response to Wnt signalling in early Xenopus is not brought about by differential use of distinct signal transduction pathways. In fact β-catenin, a downstream component of the canonical Wnt signal transduction pathway, functions not only in the early dorsalising response but also in the later ventrolateral-promoting response. Interaction of β-catenin with the XTcf-3 transcription factor is required for the early dorsalising activity. In contrast, our experiments suggest that late Wnt signalling in the ventrolateral mesoderm does not require a similar dependency of β-catenin function on XTcf-3. Our results highlight the potential versatility of the canonical Wnt pathway to interact with tissue-specific factors downstream of β-catenin, in order to achieve tissue-specific effects.

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