A role foriro1andiro7in the establishment of an anteroposterior compartment of the ectoderm adjacent to the midbrain-hindbrain boundary

Development ◽  
2002 ◽  
Vol 129 (10) ◽  
pp. 2317-2327 ◽  
Author(s):  
Motoyuki Itoh ◽  
Tetsuhiro Kudoh ◽  
Michael Dedekian ◽  
Cheol-Hee Kim ◽  
Ajay B. Chitnis

We have identified a novel Iroquois (Iro) gene, iro7, in zebrafish. iro7 is expressed during gastrulation along with iro1 in a compartment of the dorsal ectoderm that includes the prospective midbrain-hindbrain domain, the adjacent neural crest and the trigeminal placodes in the epidermis. The iro1 and iro7 expression domain is expanded in headless and masterblind mutants, which are characterized by exaggerated Wnt signaling. Early expansion of iro1 and iro7 expression in these mutants correlates with expansion of the midbrain-hindbrain boundary (MHB) domain, the neural crest and trigeminal neurons, raising the possibility that iro1 and iro7 have a role in determination of these ectodermal derivatives. A knockdown of iro7 function revealed that iro7 is essential for the determination of neurons in the trigeminal placode. In addition, a knockdown of both iro1 and iro7 genes uncovered their essential roles in neural crest development and establishment of the isthmic organizer at the MHB. These results suggest a new role for Iro genes in establishment of an ectodermal compartment after Wnt signaling in vertebrate development. Furthermore, analysis of activator or repressor forms of iro7 suggests that iro1 and iro7 are likely to function as repressors in establishment of the isthmic organizer and neural crest, and Iro genes may have dual functions as repressors and activators in neurogenesis.

2007 ◽  
Vol 306 (1) ◽  
pp. 318-319
Author(s):  
Roberto Mayor ◽  
Helen Matthews ◽  
Lorena Marchant ◽  
Carlos Carmona-Fontaine ◽  
Sei Kuriyama

2021 ◽  
Vol 12 ◽  
Author(s):  
Erica J. Hutchins ◽  
Michael L. Piacentino ◽  
Marianne E. Bronner

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.


Development ◽  
2001 ◽  
Vol 128 (19) ◽  
pp. 3655-3663 ◽  
Author(s):  
Matthew A. Deardorff ◽  
Change Tan ◽  
Jean-Pierre Saint-Jeannet ◽  
Peter S. Klein

Wnts are a large family of secreted molecules implicated in numerous developmental processes. Frizzled proteins are likely receptors for Wnts and are required for Wnt signaling in invertebrates. A large number of vertebrate frizzled genes have also been identified, but their roles in mediating specific responses to endogenous Wnts have not been well defined. Using a functional assay in Xenopus, we have performed a large screen to identify potential interactions between Wnts and frizzleds. We find that signaling by Xwnt1, but not other Wnts, can be specifically enhanced by frizzled 3 (Xfz3). As both Xfz3 and Xwnt1 are highly localized to dorsal neural tissues that give rise to neural crest, we examined whether Xfz3 mediates Xwnt1 signaling in the formation of neural crest. Xfz3 specifically induces neural crest in ectodermal explants and in embryos, similar to Xwnt1, and at lower levels of expression, synergizes with Xwnt1 in neural crest induction. Furthermore, loss of Xfz3 function, either by depletion with a Xfz3-directed morpholino antisense oligonucleotide or by expression of an inhibitory form of Xfz3 (Nfz3), prevents Xwnt1-dependent neural crest induction in ectodermal explants and blocks neural crest formation in whole embryos. These results show that Xfz3 is required for Xwnt1 signaling in the formation of the neural crest in the developing vertebrate embryo.


2019 ◽  
Author(s):  
Mansour Alkobtawi ◽  
Patrick Pla ◽  
Anne H. Monsoro-Burq

AbstractHow multiple morphogen signals are coordinated in space and time to position key embryonic tissues remains elusive. During neural crest formation, bone morphogenetic protein (BMP), fibroblast growth factor (FGF) and WNT signaling cooperate by acting either on the paraxial mesoderm or directly on the neural border ectoderm, but how each tissue interprets this complex information remains poorly understood. Here we show that Fhl3, a scaffold LIM domain protein of previously unknown developmental function, is essential for neural crest formation by linking BMP and WNT signaling thereby positioning the neural crest-inducing signaling center in the paraxial mesoderm. During gastrulation, Fhl3 promotes Smad phosphorylation and Smad-dependent wnt8 activation specifically in the paraxial mesoderm, thus modifying the respective mesoderm or ectoderm cell response to the extracellular BMP gradient. This ensures neural border ectoderm specification by the underlying mesoderm via non-cell autonomous WNT signaling. During neurulation, neural crest inducers activate fhl3, promoting BMP/Smad-dependent WNT activity required for neural crest specification. Our findings highlight how Fhl3, acting cell-autonomously, ensures a fine spatial, temporal and germ layer-specific coordination of BMP and WNT signaling at several steps of neural crest development.Highlights:-FHL3 is a novel intracellular enhancer of BMP signaling during early development.-FHL3 ensures cross-talk between BMP and WNT signaling by Smad1-dependent wnt8 activation in the paraxial mesoderm.-FHL3 reiterated function in paraxial mesoderm and in neural border ectoderm is essential for neural crest development at the border of the neural plate.


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