Frizzled-7 signalling controls tissue separation during Xenopus gastrulation

Winklbauer, Rudolf; Medina, Araceli; Swain, Roy; Steinbeißer, Herbert

doi:10.1038/35101621

Cited by 244 publications

(228 citation statements)

References 21 publications

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“…Inhibition of canonical Wnt signalling by a dominant-negative form of Tcf3 does not inhibit neural crest migration (F. Romero and R.M., unpublished). There is convincing experimental evidence that shows that canonical Wnt signalling is involved in neural crest induction and cell differentiation (Dorsky et al, 1998;Garcia-Castro et al, 2002;LaBonne and Bronner-Fraser, 1998;Lee et al, 2004 (CarreiraBarbosa et al, 2003;Djiane et al, 2000;Kuhl et al, 2000;Medina et al, 2000;Sumanas and Ekker, 2001;Wang and Malbon, 2004;Winklbauer et al, 2001). We have shown that Fz7 is expressed in the premigratory neural crest just before migration, as well as in the migrating neural crest.…”

Section: Discussionmentioning

confidence: 86%

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Essential role of non-canonical Wnt signalling in neural crest migration

et al. 2005

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Migration of neural crest cells is an elaborate process that requires the delamination of cells from an epithelium and cell movement into an extracellular matrix. In this work, it is shown for the first time that the non-canonical Wnt signalling [planar cell polarity (PCP) or Wnt-Ca2+] pathway controls migration of neural crest cells. By using specific Dsh mutants, we show that the canonical Wnt signalling pathway is needed for neural crest induction, while the non-canonical Wnt pathway is required for neural crest migration. Grafts of neural crest tissue expressing non-canonical Dsh mutants, as well as neural crest cultured in vitro, indicate that the PCP pathway works in a cell-autonomous manner to control neural crest migration. Expression analysis of non-canonical Wnt ligands and their putative receptors show that Wnt11 is expressed in tissue adjacent to neural crest cells expressing the Wnt receptor Frizzled7 (Fz7). Furthermore, loss- and gain-of-function experiments reveal that Wnt11 plays an essential role in neural crest migration. Inhibition of neural crest migration by blocking Wnt11 activity can be rescued by intracellular activation of the non-canonical Wnt pathway. When Wnt11 is expressed opposite its normal site of expression, neural crest migration is blocked. Finally, time-lapse analysis of cell movement and cell protrusion in neural crest cultured in vitro shows that the PCP or Wnt-Ca2+ pathway directs the formation of lamellipodia and filopodia in the neural crest cells that are required for their delamination and/or migration.

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Section: Discussionmentioning

confidence: 86%

“…Although no specific Wnt11 receptor has been identified, there is some evidence that suggests that PCP Wnt signalling involves Fz7 (Carreira-Barbosa et al, 2003;Djiane et al, 2000;Medina et al, 2000;Sumanas and Ekker, 2001;Winklbauer et al, 2001). We examined the distribution of the Fz7 receptor in neural crest cells.…”

Section: Resultsmentioning

confidence: 99%

Essential role of non-canonical Wnt signalling in neural crest migration

et al. 2005

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“…During development, FZD7-mediated tissue movement or cell migration involves non-canonical Wnt signalling. For example, neural crest cell migration in birds is mediated by Wnt11/FZD7 (De Calisto et al, 2005); and tissue separation (Winklbauer et al, 2001) and convergent extension movements (Djiane et al, 2000) during Xenopus gastrulation are via FZD7-mediated noncanonical Wnt/Ca 2 þ and Wnt/PCP pathways, respectively (reviewed in Kuhl, 2002;Tada et al, 2002). In contrast, FZD7-mediated tissue construction or epithelialization involves canonical Wnt signalling.…”

Section: Discussionmentioning

confidence: 99%

“…Frizzled-7 (FZD7) is a seven-pass trans-membrane Wnt receptor that governs developmental morphogenetic events such as gastrulation (Winklbauer et al, 2001;Tada et al, 2002). Gastrulation is a series of coordinated movements of cell groups to establish the basic body plan of vertebrate embryos and as such involves remarkable changes in cell morphology, cell adhesion, cell-cell junction and cell mobility.…”

Section: Introductionmentioning

confidence: 99%

Frizzled-7 dictates three-dimensional organization of colorectal cancer cell carcinoids

et al. 2006

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Progression of colorectal cancer (CRC) involves spatial and temporal occurrences of epithelial-mesenchymal transition (EMT), whereby tumour cells acquire a more invasive and metastatic phenotype. Subsequently, the disseminated mesenchymal tumour cells must undergo a reverse transition (mesenchymal-epithelial transition, MET) at the site of metastases, as most metastases recapitulate the pathology of their corresponding primary tumours. Importantly, initiation of tumour growth at the secondary site is the rate-limiting step in metastasis. However, investigation of this dynamic reversible EMT and MET that underpins CRC morphogenesis has been hindered by a lack of suitable in vitro models. To this end, we have established a unique in vitro model of CRC morphogenesis, which we term LIM1863-Mph (morphogenetic). LIM1863-Mph cells spontaneously undergo cyclic transitions between two-dimensional monolayer (migratory, mesenchymal) and three-dimensional sphere (carcinoid, epithelial) states. Using RNAi, we demonstrate that FZD7 is necessary for MET of the monolayer cells as loss of FZD7 results in the persistence of a mesenchymal state (increased SNAI2/decreased E-cadherin). Moreover, FZD7 is also required for migration of the LIM1863-Mph monolayer cells. During development, FZD7 orchestrates either migratory or epithelialization events depending on the context. Our findings strongly implicate similar functional diversity for FZD7 during CRC morphogenesis.

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“…Many of FZD receptors, including FZD3 and FZD7, are able to activate the canonical b-catenin pathway, whereas data are not so obvious for FZD6. The noncanonical PKC and JNK pathways have been clearly shown as potentially activated by some FZD family members as FZD7, whereas it remains ambiguous for FZD3 and FZD6 (He et al, 1998;Winklbauer et al, 2001;Kinoshita et al, 2003;Merle et al, 2004;Katoh, 2007;Katoh and Katoh, 2007b). We have previously reported that the FZD7-mediated signalling was able to control the cancerous phenotype of human HCC cell lines through b-catenin protein regulation, and that one of the Wnt ligand candidate activators is WNT3 (Merle et al, 2004(Merle et al, , 2005Kim et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Common dysregulation of Wnt/Frizzled receptor elements in human hepatocellular carcinoma

et al. 2008

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Dysregulation of growth factors and their receptors is central to human hepatocellular carcinoma (HCC). We previously demonstrated that the Frizzled-7 membrane receptor mediating the Wnt signalling can activate the b-catenin pathway and promotes malignancy in human hepatitis B virus-related HCCs. Expression patterns of all the 10 Frizzled receptors, and their extracellular soluble autoparacrine regulators (19 Wnt activators and 4 sFRP inhibitors) were assessed by real-time RT -PCR in 62 human HCC of different etiologies and their matched peritumorous areas. Immunostaining was performed to localise Frizzled on cell types in liver tissues. Regulation of three known Frizzled-dependent pathways (b-catenin, protein kinase C, and C-Jun NH 2 -terminal kinase) was measured in tissues by western blot. We found that eight Frizzled-potentially activating events were pleiotropically dysregulated in 95% HCC and 68% peritumours as compared to normal livers (upregulations of Frizzled-3/6/7 and Wnt3/4/5a, or downregulation of sFRP1/5), accumulating gradually with severity of fibrosis in peritumours and loss of differentiation status in tumours. The hepatocytes supported the Wnt/Frizzled signalling since specifically overexpressing Frizzled receptors in liver tissues. Dysregulation of the eight Frizzled-potentially activating events was associated with differential activation of the three known Frizzled-dependent pathways. This study provides an extensive analysis of the Wnt/Frizzled receptor elements and reveals that the dysregulation may be one of the most common and earliest events described thus far during hepatocarcinogenesis.

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Frizzled-7 signalling controls tissue separation during Xenopus gastrulation

Cited by 244 publications

References 21 publications

Essential role of non-canonical Wnt signalling in neural crest migration

Essential role of non-canonical Wnt signalling in neural crest migration

Frizzled-7 dictates three-dimensional organization of colorectal cancer cell carcinoids

Common dysregulation of Wnt/Frizzled receptor elements in human hepatocellular carcinoma

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