Abstract
Canonical Wnt signaling converts the TCF/LEF transcription factor from repressor to activator by increasing nuclear levels of its coactivator, β-catenin. A striking exception had been reported for Wnt-induced endoderm formation during C. elegans embryogenesis. It has long been believed that transcriptional activation of Wnt target genes in the endoderm precursor occurred due to a lowering of nuclear levels of the worm TCF/LEF protein, POP-1, effectively alleviating POP-1 repressive activity. Contrary to this model, we demonstrate here that POP-1 directly activates Wnt target genes in the endoderm precursor. Wnt converts POP-1 from a repressor to an activator, and this conversion requires that POP-1 nuclear levels be lowered in the endoderm precursor. We propose that the balance between TCF/LEF and coactivator(s), achieved by elevating coactivator levels (the canonical pathway) and/or reducing TCF/LEF levels (worm endoderm), determines Wnt signal strength.
Original language | English (US) |
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Pages (from-to) | 584-592 |
Number of pages | 9 |
Journal | Developmental Biology |
Volume | 285 |
Issue number | 2 |
DOIs | |
State | Published - Sep 15 2005 |
Keywords
- C. elegans
- Endoderm
- POP-1
- TCF/LEF
- Wnt
- β-catenin
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology