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Canonical and non‐canonical Wnt signaling pathways in Caenorhabditis elegans : variations on a common signaling theme
Author(s) -
Korswagen Hendrik C.
Publication year - 2002
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/bies.10145
Subject(s) - wnt signaling pathway , biology , lrp5 , microbiology and biotechnology , lrp6 , frizzled , signal transduction , caenorhabditis elegans , cell fate determination , endoderm , beta catenin , genetics , cell polarity , transcription factor , cellular differentiation , gene , cell
Wnt glycoproteins are signaling molecules that control a wide range of developmental processes in organisms ranging from the simple metazoan Hydra to vertebrates. Wnt signaling also plays a key role in the development of the nematode C. elegans , and is involved in cell fate specification and determination of cell polarity and cell migration. Surprisingly, the first genetic studies of Wnt signaling in C. elegans revealed major differences with the established (canonical) Wnt signaling pathways of Drosophila and vertebrates. Thus, the Wnt‐dependent induction of endoderm in the early embryo and the specification of several asymmetric cell divisions during larval development are mediated by as yet novel Wnt signaling pathways that repress, rather than activate the TCF/LEF‐1 transcription factor POP‐1. Recently, however, it has been shown that, in addition to these divergent Wnt pathways, C. elegans also has a canonical Wnt pathway that converts POP‐1 into an activator and controls the expression of several homeobox genes. Interestingly, these different Wnt pathways use distinct β‐catenins to control POP‐1 function: the endoderm induction pathway requires the β‐catenin WRM‐1 and parallel input from a mitogen‐activated kinase (MAPK) pathway to downregulate POP‐1, whereas the canonical Wnt pathway employs the β‐catenin BAR‐1 to activate Wnt target gene expression. BioEssays 24:801–810, 2002. © 2002 Wiley Periodicals, Inc.