Cdo suppresses canonical Wnt signalling via interaction with Lrp6 thereby promoting neuronal differentiation

Myong-Ho Jeong, Seok-Man Ho, Tuan Anh Vuong, Shin-Bum Jo, Guizhong Liu, Stuart A. Aaronson, Young-Eun Leem and Jong-Sun Kang ()
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Myong-Ho Jeong: Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute
Seok-Man Ho: Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute
Tuan Anh Vuong: Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute
Shin-Bum Jo: Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute
Guizhong Liu: Icahn School of Medicine at Mount Sinai
Stuart A. Aaronson: Icahn School of Medicine at Mount Sinai
Young-Eun Leem: Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute
Jong-Sun Kang: Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Canonical Wnt signalling regulates expansion of neural progenitors and functions as a dorsalizing signal in the developing forebrain. In contrast, the multifunctional co-receptor Cdo promotes neuronal differentiation and is important for the function of the ventralizing signal, Shh. Here we show that Cdo negatively regulates Wnt signalling during neurogenesis. Wnt signalling is enhanced in Cdo-deficient cells, leading to impaired neuronal differentiation. The ectodomains of Cdo and Lrp6 interact via the Ig2 repeat of Cdo and the LDLR repeats of Lrp6, and the Cdo Ig2 repeat is necessary for Cdo-dependent Wnt inhibition. Furthermore, the Cdo-deficient dorsal forebrain displays stronger Wnt signalling activity, increased cell proliferation and enhanced expression of the dorsal markers and Wnt targets, Pax6, Gli3, Axin2. Therefore, in addition to promoting ventral central nervous system cell fates with Shh, Cdo promotes neuronal differentiation by suppression of Wnt signalling and provides a direct link between two major dorsoventral morphogenetic signalling pathways.

Date: 2014
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DOI: 10.1038/ncomms6455

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