scholarly journals FGF and canonical Wnt signaling cooperate to induce paraxial mesoderm from tailbud neuromesodermal progenitors through regulation of a two-step epithelial to mesenchymal transition

Development ◽  
2017 ◽  
Vol 144 (8) ◽  
pp. 1412-1424 ◽  
Author(s):  
Hana Goto ◽  
Samuel C. Kimmey ◽  
Richard H. Row ◽  
David Q. Matus ◽  
Benjamin L. Martin
Keyword(s):  
Wnt Signaling ◽  
Epithelial To Mesenchymal Transition ◽  
Paraxial Mesoderm ◽  
Canonical Wnt Signaling ◽  
Mesenchymal Transition ◽  
Canonical Wnt

scholarly journals Draxin acts as a molecular rheostat of canonical Wnt signaling to control cranial neural crest EMT

2018 ◽  
Vol 217 (10) ◽  
pp. 3683-3697 ◽  
Author(s):  
Erica J. Hutchins ◽  
Marianne E. Bronner
Keyword(s):  
Wnt Signaling ◽  
Neural Crest ◽  
Neural Tube ◽  
Epithelial To Mesenchymal Transition ◽  
Cranial Neural Crest ◽  
Canonical Wnt Signaling ◽  
Mesenchymal Transition ◽  
Molecular Rheostat ◽  
Timing Of Initiation ◽  
Canonical Wnt

Neural crest cells undergo a spatiotemporally regulated epithelial-to-mesenchymal transition (EMT) that proceeds head to tailward to exit from the neural tube. In this study, we show that the secreted molecule Draxin is expressed in a transient rostrocaudal wave that mirrors this emigration pattern, initiating after neural crest specification and being down-regulated just before delamination. Functional experiments reveal that Draxin regulates the timing of cranial neural crest EMT by transiently inhibiting canonical Wnt signaling. Ectopic maintenance of Draxin in the cranial neural tube blocks full EMT; while cells delaminate, they fail to become mesenchymal and migratory. Loss of Draxin results in premature delamination but also in failure to mesenchymalize. These results suggest that a pulse of intermediate Wnt signaling triggers EMT and is necessary for its completion. Taken together, these data show that transient secreted Draxin mediates proper levels of canonical Wnt signaling required to regulate the precise timing of initiation and completion of cranial neural crest EMT.

scholarly journals Sox2 and canonical Wnt signaling interact to activate a developmental checkpoint coordinating morphogenesis with mesodermal fate acquisition

2020 ◽  
Author(s):  
Brian A. Kinney ◽  
Richard H. Row ◽  
Yu-Jung Tseng ◽  
Maxwell D. Weidmann ◽  
Holger Knaut ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Cell Fate ◽  
Epithelial To Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Mesoderm Induction ◽  
Cell Fate Specification ◽  
Canonical Wnt Signaling ◽  
Mesodermal Cell ◽  
Mesenchymal Transition ◽  
Canonical Wnt

AbstractAnimal embryogenesis requires a precise coordination between morphogenesis and cell fate specification. It is unclear if there are mechanisms that prevent uncoupling of these processes to ensure robust development. During mesoderm induction, mesodermal fate acquisition is tightly coordinated with the morphogenetic process of epithelial to mesenchymal transition (EMT). In zebrafish, cells exist transiently in a partial EMT state during mesoderm induction. Here we show that cells expressing the neural inducing transcription factor Sox2 are held in the partial EMT state, stopping them from completing the EMT and joining the mesodermal territory. This is critical for preventing ectopic neural tissue from forming. The mechanism involves specific interactions between Sox2 and the mesoderm inducing canonical Wnt signaling pathway. When Wnt signaling is inhibited in Sox2 expressing cells trapped in the partial EMT, cells are now able to exit into the mesodermal territory, but form an ectopic spinal cord instead of mesoderm. Our work identifies a critical developmental checkpoint that ensures that morphogenetic movements establishing the mesodermal germ layer are accompanied by robust mesodermal cell fate acquisition.

scholarly journals A Novel sLRP6E1E2 Inhibits Canonical Wnt Signaling, Epithelial-to-Mesenchymal Transition, and Induces Mitochondria-Dependent Apoptosis in Lung Cancer

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e36520 ◽  
Author(s):  
Jung-Sun Lee ◽  
Man-Wook Hur ◽  
Seong Kyung Lee ◽  
Won-Il Choi ◽  
Young-Guen Kwon ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Wnt Signaling ◽  
Epithelial To Mesenchymal Transition ◽  
Canonical Wnt Signaling ◽  
Mesenchymal Transition ◽  
Canonical Wnt

scholarly journals Transcriptomic Identification of Draxin-Responsive Targets During Cranial Neural Crest EMT

2021 ◽  
Vol 12 ◽  
Author(s):  
Erica J. Hutchins ◽  
Michael L. Piacentino ◽  
Marianne E. Bronner
Keyword(s):  
Wnt Signaling ◽  
Neural Crest ◽  
Gene List ◽  
Hybridization Chain Reaction ◽  
Cranial Neural Crest ◽  
Canonical Wnt Signaling ◽  
Chain Reaction ◽  
Mesenchymal Transition ◽  
Neural Crest Development ◽  
Canonical Wnt

Canonical Wnt signaling plays an essential role in proper craniofacial morphogenesis, at least partially due to regulation of various aspects of cranial neural crest development. In an effort to gain insight into the etiology of craniofacial abnormalities resulting from Wnt signaling and/or cranial neural crest dysfunction, we sought to identify Wnt-responsive targets during chick cranial neural crest development. To this end, we leveraged overexpression of a canonical Wnt antagonist, Draxin, in conjunction with RNA-sequencing of cranial neural crest cells that have just activated their epithelial–mesenchymal transition (EMT) program. Through differential expression analysis, gene list functional annotation, hybridization chain reaction (HCR), and quantitative reverse transcription polymerase chain reaction (RT-qPCR), we validated a novel downstream target of canonical Wnt signaling in cranial neural crest – RHOB – and identified possible signaling pathway crosstalk underlying cranial neural crest migration. The results reveal novel putative targets of canonical Wnt signaling during cranial neural crest EMT and highlight important intersections across signaling pathways involved in craniofacial development.

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