Controlled levels of canonical Wnt signaling are required for neural crest migration

Maj, Ewa; Künneke, Lutz; Loresch, Elisabeth; Grund, Anita; Melchert, Juliane; Pieler, Tomas; Aspelmeier, Timo; Borchers, Annette

doi:10.1016/j.ydbio.2016.06.022

Cited by 41 publications

(43 citation statements)

References 277 publications

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“…Neural crest cells also provide an explanation for the relevance of the inhibition of canonical Wnt signaling by PTK7. Canonical Wnt activity decreases at the onset of neural crest migration, and ectopic activation inhibits neural crest migration (Maj et al, 2016;Rabadán et al, 2016). Thus, neural crest cells require controlled basal levels of canonical Wnt signaling to enable their migration.…”

Section: Discussionmentioning

confidence: 99%

PTK7 localization and protein stability is affected by canonical Wnt ligands

Berger

Breuer

Peradziryi

et al. 2017

Journal of Cell Science

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Protein tyrosine kinase 7 (PTK7) is an evolutionarily conserved transmembrane receptor with important roles in embryonic development and disease. Originally identified as a gene upregulated in colon cancer, it was later shown to regulate planar cell polarity (PCP) and directional cell movement. PTK7 is a Wnt co-receptor; however, its role in Wnt signaling remains controversial. Here, we find evidence that places PTK7 at the intersection of canonical and non-canonical Wnt signaling pathways. In presence of canonical Wnt ligands PTK7 is subject to caveolin-mediated endocytosis, while it is unaffected by non-canonical Wnt ligands. PTK7 endocytosis is dependent on the presence of the PTK7 co-receptor Fz7 (also known as Fzd7) and results in lysosomal degradation of PTK7. As we previously observed that PTK7 activates non-canonical PCP Wnt signaling but inhibits canonical Wnt signaling, our data suggest a mutual inhibition of canonical and PTK7 Wnt signaling. PTK7 likely suppresses canonical Wnt signaling by binding canonical Wnt ligands thereby preventing their interaction with Wnt receptors that would otherwise support canonical Wnt signaling. Conversely, if canonical Wnt proteins interact with the PTK7 receptor, they induce its internalization and degradation.

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Section: Discussionmentioning

confidence: 99%

PTK7 localization and protein stability is affected by canonical Wnt ligands

Berger

Breuer

Peradziryi

et al. 2017

Journal of Cell Science

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“…While the Wnt/β-catenin pathway is critical for the specification of the neural crest (Simoes-Costa and Bronner, 2015). More recently, it has been reported that the Wnt/β-catenin signaling pathway need to be carefully regulated during CNC migration in frogs (Maj et al, 2016). Cadherin-11 overexpression reduces the pool of β-catenin available for Wnt signaling pathway.…”

Section: E-cadherin Versus N-cadherin: Switch or Change In Function?mentioning

confidence: 99%

Cadherins function during the collective cell migration of Xenopus Cranial Neural Crest cells: revisiting the role of E-cadherin

Cousin

2017

Mechanisms of Development

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Collective cell migration is a process whereby cells move while keeping contact with other cells. The Xenopus Cranial Neural Crest (CNC) is a population of cells that emerge during early embryogenesis and undergo extensive migration from the dorsal to ventral part of the embryo’s head. These cells migrate collectively and require cadherin mediated cell-cell contact. In this review, we will describe the key features of Xenopus CNC migration including the key molecules driving their migration. We will also review the role of the various cadherins during Xenopus CNC emergence and migration. Lastly, we will discuss the recent and seemingly controversial findings showing that E-cadherin presence is essential for CNC migration.

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“…This process is regulated at multiple levels. At the signaling level, canonical Wnt signaling and Bone Morphogenic Protein signaling need to be tightly controlled to allow for the migration of NCCs (Burstyn-Cohen et al, 2004; Ulmer et al, 2013; Maj et al, 2016). Downstream of these signaling pathways, several tiers of transcription factors are activated in NCCs.…”

Section: Introductionmentioning

confidence: 99%