Abstract

The use of Wnt ligands for signaling between cells is a conserved feature of metazoan development. Activation of Wnt signal transduction pathways upon ligand binding can regulate diverse processes including cell proliferation, migration, polarity, differentiation and axon outgrowth. A 'canonical' Wnt signaling pathway has been elucidated in vertebrate and invertebrate model systems. In the canonical pathway, Wnt binding leads to the stabilization of the transcription factor beta-catenin, which enters the nucleus to regulate Wnt pathway target genes. However, Wnt binding also acts through beta-catenin-independent, noncanonical pathways, such as the planar cell polarity (PCP) pathway and a pathway involving Ca2+ signaling. This chapter examines our current understanding of Wnt signaling and Wnt-mediated processes in the nematode C. elegans. Like other species, the C. elegans genome encodes multiple genes for Wnt ligands (five) and Wnt receptors (four frizzleds, one Ryk/Derailed). Unlike vertebrates or Drosophila, the C. elegans genome encodes three beta-catenin genes, which appear to have distinct functions in Wnt signaling and cell adhesion. Canonical Wnt signaling clearly exists in C. elegans, utilizing the beta-catenin BAR-1. However, a noncanonical pathway utilizing the beta-catenin WRM-1 also exists, and to date a similar pathway has not been described in other species. Evidence for beta-catenin independent noncanonical Wnt signaling is currently limited. The role of Wnt signaling in over a dozen C. elegans developmental processes, including the regulation of cell fate, polarity and migration, is described.

Highlights

  • The Wnt extracellular signaling pathway is one of a handful of evolutionarily-conserved signal transduction pathways used extensively during animal development, from Hydra to humans (Cadigan and Nusse, 1997; Wodarz and Nusse, 1998; Hobmayer et al, 2000; Peifer and Polakis, 2000)

  • This phenomenon is likely related to a second difference, which is that for the Z1/Z4 and T cell processes, loss of pop-1/TCF gives the same phenotype as loss of wrm-1/β-cat or lit-1/Nlk, but for P2-EMS signaling loss of pop-1/TCF activity gives the opposite phenotype. This would be expected if in the former cases Wnt signaling leads to an active, low abundance form of POP-1, while in the latter case Wnt signaling removes active POP-1 from the nucleus. These results indicate that in C. elegans there is variability in how the same components are utilized within noncanonical Wnt signaling pathways

  • The β-catenin-independent process of spindle reorientation may represent the first example of a noncanonical Wnt pathway in C. elegans similar to those seen in other species

Read more

Summary

Introduction

The Wnt extracellular signaling pathway (wingless in Drosophila) is one of a handful of evolutionarily-conserved signal transduction pathways used extensively during animal development, from Hydra to humans (Cadigan and Nusse, 1997; Wodarz and Nusse, 1998; Hobmayer et al, 2000; Peifer and Polakis, 2000). Wnt signals control multiple aspects of development, including the proliferation, fate specification, polarity, and migration of cells. Overactivation of Wnt signaling by mutation is a major factor in oncogenesis in the human colon and other tissues (Polakis, 2000). Work in Drosophila and vertebrates has shown that Wnt signals are transduced in at least two distinct ways; a well-established 'canonical' or Wnt/β-catenin pathway, and a noncanonical pathway or pathways that are β-catenin independent

Canonical and noncanonical Wnt signaling in flies and vertebrates
P12 fate specification
Postdereid formation from V5
Ray formation from V5 in the male tail
Differences in noncanonical pathways
Spindle reorientation in embryogenesis
POP-1 asymmetry in AB embryonic lineages
HSN migration
V5 polarity
Spicule development
Conclusion
Findings
11. References

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.