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Deficiency of the Wnt receptor Ryk causes multiple cardiac and outflow tract defects

Kumudhini Kugathasan1,2, Michael M Halford1,3, Peter G Farlie4

  • 1a Ludwig Institute for Cancer Research , Royal Melbourne Hospital , Melbourne , Australia.

Growth Factors (Chur, Switzerland)
|July 24, 2018
PubMed

Insights

Ryk, a pseudokinase, is essential for normal heart development. Ryk deficiency in mice causes congenital heart defects, revealing its role in cardiovascular morphogenesis.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Ryk is a receptor tyrosine kinase (RTK) family member that binds Wnt ligands.
  • Ryk lacks intrinsic protein tyrosine kinase activity, classifying it as a pseudokinase.
  • RTKs regulate cellular processes, but Ryk's specific role in development is unclear.

Purpose of the Study:

  • To investigate the role of Ryk in mammalian cardiac development.
  • To characterize cardiovascular and pharyngeal defects in Ryk-deficient mice.
  • To elucidate the connection between Ryk, Wnt signaling, and heart formation.

Main Methods:

  • Examination of Ryk-deficient (Ryk-/-) mice.
  • Vascular corrosion casting.
  • Vascular perfusion with contrast dye.
  • Immunohistochemistry.

Main Results:

  • Ryk-/- embryos exhibit significant cardiovascular malformations.
  • Defects include aortic arch stenosis/interruption, ventriculoarterial malalignment, and ventricular septal defects.
  • Abnormal pharyngeal arch artery remodeling was also observed.

Conclusions:

  • Ryk plays a critical role in directing morphogenetic events during cardiac development.
  • Ryk deficiency recapitulates features of human congenital heart defects.
  • This study highlights Ryk's function at the intersection of planar cell polarity signaling, Wnt ligands, and mammalian cardiovascular development.
Keywords:
Cardiovascular developmentRykWnt signallinggrowth factor receptorheart defects

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