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Updated: Aug 17, 2026

Microbead Implantation in the Zebrafish Embryo
Published on: July 30, 2015
FGF signal regulates gastrulation cell movements and morphology through its target NRH
Hyeyoung A Chung1, Junko Hyodo-Miura, Teruyuki Nagamune
1Department of Developmental Biology, National Institute for Basic Biology, 38 Nishigonaka, Myodaiji, Okazaki 444-8585, Japan.
Abstract:
We used cDNA microarray analysis to screen for FGF target genes in Xenopus embryos treated with the FGFR1 inhibitor SU5402, and identified neurotrophin receptor homolog (NRH) as an FGF target. Causing gain of NRH function by NRH mRNA or loss of NRH function using a Morpholino antisense-oligonucleotide (Mo) led to gastrulation defects without affecting mesoderm differentiation. Depletion of NRH by the Mo perturbed the polarization of cells in the dorsal marginal zone (DMZ), thereby inhibiting the intercalation of the cells during convergent extension as well as the filopodia formation on DMZ cells. Deletion analysis showed that the carboxyl-terminal region of NRH, which includes the "death domain," was necessary and sufficient to rescue gastrulation defects and to induce the protrusive cell morphology. Furthermore, we found that the FGF signal was both capable of inducing filopodia in animal cap cells, where they do not normally form, and necessary for filopodia formation in DMZ cells. Finally, we demonstrated that FGF required NRH function to induce normal DMZ cell morphology. This study is the first to identify an in vivo role for FGF in the regulation of cell morphology, and we have linked this function to the control of gastrulation cell movements via NRH.
Insights
Fibroblast Growth Factor (FGF) signaling regulates cell morphology and gastrulation movements in Xenopus embryos through neurotrophin receptor homolog (NRH). NRH depletion disrupts cell polarization and filopodia formation, essential for embryonic development.
Area of Science:
- Developmental Biology
- Cell Biology
- Molecular Biology
Background:
- Fibroblast Growth Factor (FGF) signaling plays crucial roles in embryonic development.
- The precise mechanisms by which FGF regulates cell morphology and movements during gastrulation are not fully understood.
Purpose of the Study:
- To identify FGF target genes involved in Xenopus gastrulation.
- To elucidate the role of neurotrophin receptor homolog (NRH) in FGF-mediated cell morphology and gastrulation.
Main Methods:
- cDNA microarray analysis to screen for FGF target genes.
- Gain- and loss-of-function studies using NRH mRNA and Morpholino antisense-oligonucleotides (Mo).
- Deletion analysis of NRH and assessment of filopodia formation and cell morphology.
Main Results:
- Neurotrophin receptor homolog (NRH) was identified as an FGF target gene.
- NRH depletion caused gastrulation defects by impairing cell polarization, intercalation, and filopodia formation in the dorsal marginal zone.
- The carboxyl-terminal region of NRH, including the death domain, is critical for rescuing gastrulation defects and inducing protrusive cell morphology.
- FGF signaling is necessary and sufficient for filopodia formation and requires NRH to regulate dorsal marginal zone cell morphology.
Conclusions:
- FGF signaling regulates cell morphology in vivo during Xenopus gastrulation through NRH.
- NRH is a key mediator of FGF's effects on cell shape and movement, linking FGF signaling to gastrulation cell dynamics.
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