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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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The polycystin complex mediates Wnt/Ca(2+) signalling.

Seokho Kim1, Hongguang Nie1,2, Vasyl Nesin1

  • 1Department of Cell Biology, University of Oklahoma Health Sciences Center, 975 NE 10th Street, Oklahoma City, OK 73104, USA.

Nature Cell Biology
|May 24, 2016
PubMed
Summary
This summary is machine-generated.

WNT ligands bind to Polycystin-1 (PKD1) and activate calcium (Ca2+) signaling via TRPP2 channels. This discovery reveals a new role for PKD1 in WNT signaling and sheds light on Autosomal Dominant Polycystic Kidney Disease (ADPKD) causes.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • WNT ligands are crucial signaling molecules.
  • Polycystin-1 (PKD1) and TRPP2 form a complex implicated in Autosomal Dominant Polycystic Kidney Disease (ADPKD).
  • The precise function of the PKD1-TRPP2 complex in WNT signaling remains unclear.

Purpose of the Study:

  • To investigate the interaction between WNT ligands and the PKD1-TRPP2 complex.
  • To determine the role of this interaction in calcium (Ca2+) signaling.
  • To explore the implications for ADPKD pathogenesis.

Main Methods:

  • Binding assays to detect WNT-PKD1 interaction.
  • Electrophysiology to measure whole-cell currents and Ca2+ influx.
  • Analysis of patient-derived mutations in PKD1 and PKD2.
  • Cell migration and polarization assays in fibroblasts.
  • Gene manipulation studies in Xenopus embryos.

Main Results:

  • WNTs bind to the extracellular domain of PKD1, inducing TRPP2-dependent Ca2+ influx.
  • Pathogenic mutations in PKD1 or PKD2 disrupt WNT-induced signaling and complex formation.
  • Pkd2-deficient cells exhibit impaired WNT responses and cell polarization.
  • PKD1, DVL2, and WNT9A function together in tubulogenesis in Xenopus.

Conclusions:

  • PKD1 acts as a WNT (co)receptor, mediating WNT-induced Ca2+ signaling through TRPP2.
  • Defects in this WNT/Ca2+ pathway are implicated in the development of ADPKD.
  • This finding opens new avenues for understanding and potentially treating ADPKD.