Ectodermal WNT/β-catenin signaling shapes the mouse face

Reid, Bethany S.; Yang, Hui; Melvin, Vida Senkus; Taketo, Makoto Mark; Williams, Trevor

doi:10.1016/j.ydbio.2010.11.012

Cited by 83 publications

(102 citation statements)

References 39 publications

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“…However, activation of the transgenic live actin reporter R26R:Venus–actin 32 in ectoderm using an early ectoderm-specific Cre recombinase, Crect 33 , revealed that, although cell interface lengths oscillated, average AP cell interfaces did not shorten progressively during intercalation at the DV midline (average 25 som. stage AP cell interface length at T = 0 min and T = 120 min: 7.44 μm ± 0.34 μm (s.e.m.)…”

Section: Resultsmentioning

confidence: 99%

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Anisotropic stress orients remodelling of mammalian limb bud ectoderm

et al. 2015

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The physical forces that drive morphogenesis are not well characterized in vivo, especially among vertebrates. In the early limb bud, dorsal and ventral ectoderm converge to form the apical ectodermal ridge (AER), although the underlying mechanisms are unclear. By live imaging mouse embryos, we show that prospective AER progenitors intercalate at the dorsoventral boundary and that ectoderm remodels by concomitant cell division and neighbour exchange. Mesodermal expansion and ectodermal tension together generate a dorsoventrally biased stress pattern that orients ectodermal remodelling. Polarized distribution of cortical actin reflects this stress pattern in a β-catenin- and Fgfr2-dependent manner. Intercalation of AER progenitors generates a tensile gradient that reorients resolution of multicellular rosettes on adjacent surfaces, a process facilitated by β-catenin-dependent attachment of cortex to membrane. Therefore, feedback between tissue stress pattern and cell intercalations remodels mammalian ectoderm.

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Section: Resultsmentioning

confidence: 99%

“…No. CDB0218K, http://www.cdb.riken.jp/arg/reporter_mice.html 32 ); Crect 33 ; ZEG (Jackson Laboratory, Tg(CAG–Bgeo/GFP)21/Lbe/J); β-catenin flox (Jackson Laboratory, B6.129-Ctnnb1 tm2Kem /KnwJ ); Fgfr2 flox (Jackson Laboratory, STOCK Fgfr2 tm1Dor /J). Genotyping primers are available on the Jackson Laboratory website for each mouse line.…”

Section: Methodsmentioning

confidence: 99%

Anisotropic stress orients remodelling of mammalian limb bud ectoderm

et al. 2015

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“…Previous reports have shown that reduced canonical WNT signaling through deletion of Wnt9b or Lrp6 during craniofacial development leads to facial deformity, including CL/P, in mice (13,14). Furthermore, a strong correlation between ectodermal canonical WNT signaling and nasal process growth has been reported (39). From our observations of the patterns of SHH signaling (Ptch1-LacZ) and canonical WNT signaling (TOPgal) during craniofacial development, we found that those 2 signaling pathways complement each other during facial development (Supplemental Figure 4).…”

Section: Disruption Of the Shh Signaling Gradient During Craniofacialmentioning

confidence: 98%

Disrupting hedgehog and WNT signaling interactions promotes cleft lip pathogenesis

Kurosaka¹,

Iulianella²,

Williams³

et al. 2014

J. Clin. Invest.

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Cleft lip, which results from impaired facial process growth and fusion, is one of the most common cranio facial birth defects. Many genes are known to be involved in the etiology of this disorder; however, our under standing of cleft lip pathogenesis remains incomplete. In the present study, we uncovered a role for sonic hedgehog (SHH) signaling during lip fusion. Mice carrying compound mutations in hedgehog acyltransferase (Hhat) and patched1 (Ptch1) exhibited perturbations in the SHH gradient during frontonasal development, which led to hypoplastic nasal process outgrowth, epithelial seam persistence, and cleft lip. Further investi gation revealed that enhanced SHH signaling restricts canonical WNT signaling in the lambdoidal region by promoting expression of genes encoding WNT inhibitors. Moreover, reduction of canonical WNT signaling perturbed p63/interferon regulatory factor 6 (p63/IRF6) signaling, resulting in increased proliferation and decreased cell death, which was followed by persistence of the epithelial seam and cleft lip. Consistent with our results, mutations in genes that disrupt SHH and WNT signaling have been identified in both mice and humans with cleft lip. Collectively, our data illustrate that altered SHH signaling contributes to the etiology and pathogenesis of cleft lip through antagonistic interactions with other gene regulatory networks, including the canonical WNT and p63/IRF6 signaling pathways.

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“…Neural crest cells make up the majority of the cranial mesenchyme and make numerous contributions to the craniofacial complex, most notably to the facial mesenchyme and skeletal elements. Second, we utilized the Crect driver [22] to target recombination to cells within the surface ectoderm (Fig 1C and 1D). The developing surface ectoderm houses many signaling centers that are important for directing craniofacial development such as the frontonasal ectodermal zone (FEZ) and the nasal pits [23–27].…”

Section: Resultsmentioning

confidence: 99%

A tissue-specific role for intraflagellar transport genes during craniofacial development

et al. 2017

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Primary cilia are nearly ubiquitous, cellular projections that function to transduce molecular signals during development. Loss of functional primary cilia has a particularly profound effect on the developing craniofacial complex, causing several anomalies including craniosynostosis, micrognathia, midfacial dysplasia, cleft lip/palate and oral/dental defects. Development of the craniofacial complex is an intricate process that requires interactions between several different tissues including neural crest cells, neuroectoderm and surface ectoderm. To understand the tissue-specific requirements for primary cilia during craniofacial development we conditionally deleted three separate intraflagellar transport genes, Kif3a, Ift88 and Ttc21b with three distinct drivers, Wnt1-Cre, Crect and AP2-Cre which drive recombination in neural crest, surface ectoderm alone, and neural crest, surface ectoderm and neuroectoderm, respectively. We found that tissue-specific conditional loss of ciliary genes with different functions produces profoundly different facial phenotypes. Furthermore, analysis of basic cellular behaviors in these mutants suggests that loss of primary cilia in a distinct tissue has unique effects on development of adjacent tissues. Together, these data suggest specific spatiotemporal roles for intraflagellar transport genes and the primary cilium during craniofacial development.

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Ectodermal WNT/β-catenin signaling shapes the mouse face

Cited by 83 publications

References 39 publications

Anisotropic stress orients remodelling of mammalian limb bud ectoderm

Anisotropic stress orients remodelling of mammalian limb bud ectoderm

Disrupting hedgehog and WNT signaling interactions promotes cleft lip pathogenesis

A tissue-specific role for intraflagellar transport genes during craniofacial development

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