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Noncanonical Wnt signaling through G protein-linked PKCdelta activation promotes bone formation

Xiaolin Tu1, Kyu Sang Joeng, Keiichi I Nakayama

  • 1Department of Medicine, Washington University Medical School, St. Louis, MO 63110, USA.

Developmental Cell
|January 3, 2007
PubMed

Insights

Noncanonical Wnt signaling, specifically via Galpha(q/11) and PKCdelta, drives bone formation. This pathway is crucial for osteoblastogenesis and embryonic bone development in mice.

Area of Science:

  • Developmental Biology
  • Cell Signaling
  • Molecular Biology

Background:

  • Wnt signaling pathways regulate diverse animal development.
  • The canonical (beta-catenin-dependent) Wnt pathway's role in cell fate is established.
  • The role and intracellular mechanisms of noncanonical Wnt signaling in mammals remain unclear.

Purpose of the Study:

  • To elucidate the intracellular cascades of noncanonical Wnt signaling.
  • To establish a role for noncanonical Wnt signaling in mammalian osteoblastogenesis.
  • To identify potential therapeutic targets for promoting bone formation.

Main Methods:

  • Investigated Wnt3a signaling in murine ST2 cells.
  • Utilized Galpha(q/11) and PKCdelta in signal transduction analysis.
  • Examined PKCdelta homozygous mutant mice and Wnt7b-ablated mouse embryos.

Main Results:

  • Wnt3a activates phosphatidylinositol signaling and PKCdelta via Galpha(q/11) in ST2 cells.
  • Galpha(q/11)-PKCdelta signaling is essential for Wnt3a-induced osteoblastogenesis.
  • PKCdelta deficiency and Wnt7b ablation in mice lead to impaired embryonic bone formation.

Conclusions:

  • A novel noncanonical Wnt signaling pathway involving Galpha(q/11)-PKCdelta regulates osteoblastogenesis.
  • This pathway is critical for embryonic bone development.
  • The identified pathway presents a potential therapeutic target for bone formation disorders.

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