FGF signal regulates gastrulation cell movements and morphology through its target NRH

Chung, Hyeyoung A.; Hyodo-Miura, Junko; Nagamune, Teruyuki; Ueno, Naoto

doi:10.1016/j.ydbio.2005.02.030

Cited by 31 publications

(33 citation statements)

References 54 publications

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“…RT-PCR analysis was performed as described previously (Chung et al, 2005). Primers for the following molecules were used: NCAM (Suzuki et al, 1995); epidermal keratin I (Suzuki et al, 2010); MyoDa (Rupp and Weintraub, 1991); ODC (Agius et al, 2000); sox2, forward 5Ј-AGAACCCCAAGATGCACAAC-3Ј and reverse 5Ј-GGACATGCTGTAGGTAGGCGA-3Ј; sox17, forward 5Ј-CCGGGTAGGAACTGTACAAC-3Ј and reverse 5Ј-TAACCCAGGCTGAAGTTCTC-3Ј.…”

Section: In Situ Hybridization and Rt-pcrmentioning

confidence: 99%

Cell movements of the deep layer of non-neural ectoderm underlie complete neural tube closure in Xenopus

et al. 2012

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SUMMARYIn developing vertebrates, the neural tube forms from a sheet of neural ectoderm by complex cell movements and morphogenesis. Convergent extension movements and the apical constriction along with apical-basal elongation of cells in the neural ectoderm are thought to be essential for the neural tube closure (NTC) process. In addition, it is known that non-neural ectoderm also plays a crucial role in this process, as the neural tube fails to close in the absence of this tissue in chick and axolotl. However, the cellular and molecular mechanisms by which it functions in NTC are as yet unclear. We demonstrate here that the non-neural superficial epithelium moves in the direction of tensile forces applied along the dorsal-ventral axis during NTC. We found that this force is partly attributable to the deep layer of non-neural ectoderm cells, which moved collectively towards the dorsal midline along with the superficial layer. Moreover, inhibition of this movement by deleting integrin 1 function resulted in incomplete NTC. Furthermore, we demonstrated that other proposed mechanisms, such as oriented cell division, cell rearrangement and cell-shape changes have no or only minor roles in the non-neural movement. This study is the first to demonstrate dorsally oriented deep-cell migration in non-neural ectoderm, and suggests that a global reorganization of embryo tissues is involved in NTC.

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Section: In Situ Hybridization and Rt-pcrmentioning

confidence: 99%

Cell movements of the deep layer of non-neural ectoderm underlie complete neural tube closure in Xenopus

et al. 2012

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“…b-Galactosidase staining was performed in advance of the WISH process as described previously (Chung et al, 2005).…”

Section: In Situ Hybridization and B-galactosidase Stainingmentioning

confidence: 99%

“…RT-PCR analysis for nectin-2 expression was performed as described previously (Chung et al, 2005) with the following primers: forward, 5Ј-TAGGATCCGTGAAAGCTGATCCAAAAAAC-3Ј; reverse, 5Ј-GGAA -TTCTTACGTCTCTTTAGAGTCGTAG-3Ј.…”

Section: Rt-pcrmentioning

confidence: 99%

“…The coding sequence of N-cadherin was subcloned from XL289n05ex using PCR with the following primers: forward 5Ј-CACCATGTGCCGGAAAGAGCCCTT-3Ј and reverse 5Ј-AGTTCAG -TCGTCGCTCCCTCCGTACAT-3Ј. Xenopus laevis E-cadherin was obtained from a stage 10 cDNA library, prepared as described previously (Chung et al, 2005), using PCR with the following primers: forward 5Ј-TAGATATCACCATGGGGTTGAAGAGGCCCT-3Ј and reverse 5Ј-GCGATATCTTAATCCTCATCACCTCCATAC-3Ј. Xenopus laevis Ccadherin construct was as previously described (Lee and Gumbiner, 1995).…”

Section: Dna Constructsmentioning

confidence: 99%

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Nectin-2 and N-cadherin interact through extracellular domains and induce apical accumulation of F-actin in apical constriction of Xenopus neural tube morphogenesis

et al. 2010

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SUMMARYNeural tube formation is one of the most dynamic morphogenetic processes of vertebrate development. However, the molecules regulating its initiation are mostly unknown. Here, we demonstrated that nectin-2, an immunoglobulin-like cell adhesion molecule, is involved in the neurulation of Xenopus embryos in cooperation with N-cadherin. First, we found that, at the beginning of neurulation, nectin-2 was strongly expressed in the superficial cells of neuroepithelium. The knockdown of nectin-2 impaired neural fold formation by attenuating F-actin accumulation and apical constriction, a cell-shape change that is required for neural tube folding. Conversely, the overexpression of nectin-2 in non-neural ectoderm induced ectopic apical constrictions with accumulated Factin. However, experiments with domain-deleted nectin-2 revealed that the intracellular afadin-binding motif, which links nectin-2 and F-actin, was not required for the generation of the ectopic apical constriction. Furthermore, we found that nectin-2 physically interacts with N-cadherin through extracellular domains, and they cooperatively enhanced apical constriction by driving the accumulation of F-actin at the apical cell surface. Interestingly, the accumulation of N-cadherin at the apical surface of neuroepithelium was dependent on the presence of nectin-2, but that of nectin-2 was not affected by depletion of N-cadherin. We propose a novel mechanism of neural tube morphogenesis regulated by the two types of cell adhesion molecules.

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“…Examples of this include the overexpression of Xsprouty2, a negative regulator of Fgf signaling (Nutt et al, 2001), and the knockdowns of neurotrophin receptor homolog (NRH) and ankyrin repeat domain protein 5 (Anr5), both Fgf downstream targets (Chung et al, 2005;Chung et al, 2007), which result in the inhibition of cell movement during convergent extension. In addition, chimeric analyses of the Fgfr1-knockout mouse have shown that these mutant cells fail to move away from the primitive streak (Ciruna and Rossant, 2001;Ciruna et al, 1997).…”

Section: Research Articlementioning

confidence: 99%

Maternal-zygotic medaka mutants forfgfr1reveal its essential role in the migration of the axial mesoderm but not the lateral mesoderm

et al. 2008

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The medaka fish (Oryzias latipes) is an emerging model organism for which a variety of unique developmental mutants have now been generated. Our recent mutagenesis screening of the medaka identified headfish(hdf), a null mutant for fgf receptor 1 (fgfr1),which fails to develop structures in the trunk and tail. Despite its crucial role in early development, the functions of Fgfr1-mediated signaling have not yet been well characterized due to the complexity of the underlying ligand-receptor interactions. In our present study, we further elucidate the roles of this pathway in the medaka using the hdf (fgfr1)mutant. Because Fgfr1 is maternally supplied in fish, we first generated maternal-zygotic (MZ) mutants by transplanting homozygous hdf germ cells into sterile interspecific hybrids. Interestingly, the host hybrid fish recovered their fertility and produced donor-derived mutant progeny. The resulting MZ mutants also exhibited severe defects in their anterior head structures that are never observed in the corresponding zygotic mutants. A series of detailed analyses subsequently revealed that Fgfr1 is required for the anterior migration of the axial mesoderm, particularly the prechordal plate, in a cell-autonomous manner, but is not required for convergence movement of the lateral mesoderm. Furthermore, fgfr1 was found to be dispensable for initial mesoderm induction. The MZ hdf medaka mutant was thus found to be a valuable model system to analyze the precise role of fgfr1-mediated signaling in vertebrate early development.

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FGF signal regulates gastrulation cell movements and morphology through its target NRH

Cited by 31 publications

References 54 publications

Cell movements of the deep layer of non-neural ectoderm underlie complete neural tube closure in Xenopus

Cell movements of the deep layer of non-neural ectoderm underlie complete neural tube closure in Xenopus

Nectin-2 and N-cadherin interact through extracellular domains and induce apical accumulation of F-actin in apical constriction of Xenopus neural tube morphogenesis

Maternal-zygotic medaka mutants forfgfr1reveal its essential role in the migration of the axial mesoderm but not the lateral mesoderm

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