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Modeling Paracrine Noncanonical Wnt Signaling In Vitro
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Modeling Paracrine Noncanonical Wnt Signaling In Vitro

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Beta-arrestin and casein kinase 1/2 define distinct branches of non-canonical WNT signalling pathways

Vítĕzslav Bryja1, Alexandra Schambony, Lukás Cajánek

  • 1Laboratory of Molecular Neurobiology, Department of Medical Biochemistry & Biophysics, Karolinska Institutet, Scheeles v ag 1, S-171 77 Stockholm, Sweden.

EMBO Reports
|October 28, 2008
PubMed

Insights

Beta-arrestin (beta-arr) drives WNT/RAC-1 signaling, while casein kinases (CK1/2) act as a switch. The balance between beta-arr and CK1/2 determines non-canonical WNT pathway activation.

Area of Science:

  • Cellular signaling
  • Molecular biology
  • Biochemistry

Background:

  • Non-canonical WNT signaling pathways are complex and their regulation is not fully understood.
  • Understanding the specificity of individual non-canonical WNT pathways is crucial.

Purpose of the Study:

  • To investigate the roles of beta-arrestin (beta-arr) and casein kinases 1 and 2 (CK1 and CK2) in non-canonical WNT signaling.
  • To determine how these components regulate signaling specificity towards the small GTPase RAC-1.

Main Methods:

  • Investigated the function of beta-arrestin in WNT/RAC-1 signaling.
  • Examined the role of casein kinases in modulating RAC-1 activation.
  • Analyzed the phosphorylation of dishevelled (DVL) by casein kinases.

Main Results:

  • Beta-arrestin (beta-arr) is both sufficient and necessary for WNT/RAC-1 signaling.
  • Casein kinases (CK1 and CK2) act as a molecular switch.
  • CK1/2 phosphorylation of DVL prevents RAC-1 activation and promotes other non-canonical WNT pathways.

Conclusions:

  • The balance between beta-arrestin and casein kinases determines the activation of specific non-canonical WNT pathways.
  • This balance dictates whether WNT signaling activates RAC-1 or other downstream effectors.

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