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doi: 10.1242/10.1242/dev.00402
,
1 Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT
84132, USA
2 Laboratory of Molecular Genetics, NICHD, NIH, Bethesda, MD 20892, USA
3 Howard Hughes Medical Institute/Department of Pharmacology and Center for
Developmental Biology, University of Washington, Seattle, WA 98195, USA
Authors for correspondence (e-mail:
richard.dorsky{at}hsc.utah.edu and chitnisa@mail.nih.gov)
Accepted 17 January 2003
Caudalizing factors operate in the context of Wnt/ß-catenin signaling to induce gene expression in discrete compartments along the rostral-caudal axis of the developing vertebrate nervous system. In zebrafish, basal repression of caudal genes is achieved through the function of Headless (Hdl), a Tcf3 homolog. In this study, we show that a second Tcf3 homolog, Tcf3b, limits caudalization caused by loss of Hdl function and although this Lef/Tcf family member can rescue hdl mutants, Lef1 cannot. Wnts can antagonize repression mediated by Tcf3 and this derepression is dependent on a Tcf3 ß-catenin binding domain. Systematic changes in gene expression caused by reduced Tcf3 function help predict the shape of a caudalizing activity gradient that defines compartments along the rostral-caudal axis. In addition, Tcf3b has a second and unique role in the morphogenesis of rhombomere boundaries, indicating that it controls multiple aspects of brain development.
Key words: Tcf3b, Headless, Zebrafish, Wnt, Neural patterning, Morphogen gradient
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