Extracellular matrix components prevent neural differentiation of disaggregated Xenopus ectoderm cells

Grunz, Horst; Tacke, Lothar

doi:10.1016/0922-3371(90)90105-6

Cited by 25 publications

(12 citation statements)

References 28 publications

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“…Recently, Grunz & Tacke (1989) have shown that when Xenopus laevis blastula or early gastrula ectoderm is dissociated and the cells kept dispersed for up to 5 h prior to reaggregation, the resulting spheres of ectodermal cells differentiate autonomously into large neural structures independently of the neural inducer, while dissociated and immediately reaggregated ectoderm will only differentiate into ciliated epidermis, in accordance with the classical experiments. This autoneutralization can be prevented by cell supernatant from dissociated ectoderm, which contains extracellular matrix components (ECM) (Grunz & Tacke, 1990). The inhibiting substances contain a substantial amount of glyco-conjugated proteins, because the inhibitory effects are inactivated by phenol extraction (Grunz & Tacke, 1990).…”

Section: Possible Mechanisms Of Neural Induction By Proteasesmentioning

confidence: 99%

“…This autoneutralization can be prevented by cell supernatant from dissociated ectoderm, which contains extracellular matrix components (ECM) (Grunz & Tacke, 1990). The inhibiting substances contain a substantial amount of glyco-conjugated proteins, because the inhibitory effects are inactivated by phenol extraction (Grunz & Tacke, 1990). Although possible proteolysis of this inhibitory ECM was not discussed by the authors, limited degradation of the ECM around competent blastomeres of the ascidian embryo might be provoked by the applied 286 NEURAL INDUCTION BY PROTEASE proteases, resulting in differentiation of the ectoderm blastomeres into neural derivatives.…”

Section: Possible Mechanisms Of Neural Induction By Proteasesmentioning

confidence: 99%

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Neural differentiation in cleavage‐arrested ascidian blastomeres induced by a proteolytic enzyme.

Okado

Takahashi

1993

The Journal of Physiology

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SUMMARY1. As previously reported, ectodermal a4-2 blastomeres isolated from 8-cell embryos of the ascidian, Halocynthia roretzi or aurantium, and cultured under conditions of cleavage arrest always differentiated into an epidermal phenotype, showing long-lasting Ca2+-dependent action potentials and/or tunic on the cell surface. a4-2 blastomeres contacted by a chordamesodermal blastomere, A4-1, differentiated into a neural phenotype, characterized by fast Na+-dependent spikes. Differentiation to a similar neural phenotype occurred when isolated a42 blastomeres from H. aurantium embryos were treated with > 0 003 % subtilisin for 60 min at the 32-cell stage of the control embryo. Comparisons between induction by cell contact and induction by proteolytic enzymes were made and showed them to be similar in several respects.2. When the serine protease, subtilisin, was used as the neural inducer, neural competence of a4-2 blastomeres, measured as the percentage frequency of the induction of Na+ spikes, increased after the 32-cell stage and decreased during the gastrula stage. The time course of the neural competence was the same as that for contact with the A4-1 blastomere.3. The neural competence of four different ectodermal blastomeres isolated from the 16-cell embryo was also examined using subtilisin as a neural inducer, and by contact with the A41 blastomere from the 8-cell embryo. The competence was higher in anterior blastomeres than in posterior blastomeres for both types of induction. This regional difference in neural competence along the antero-posterior axis paralleled that expected from neural cell lineage during normal development, i.e. blastomeres with more cells of neural lineage among their derivatives showed higher competence.4. Streptomyces subtilisin inhibitor, SSI (0 1%), a specific protease inhibitor for subtilisin-type serine proteases, significantly suppressed (50%) neural induction of the ectodermal blastomere, a4-2, by contact wtih the chordamesodermal blastomere, A4-1.

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Section: Possible Mechanisms Of Neural Induction By Proteasesmentioning

confidence: 99%

Section: Possible Mechanisms Of Neural Induction By Proteasesmentioning

confidence: 99%

Neural differentiation in cleavage‐arrested ascidian blastomeres induced by a proteolytic enzyme.

Okado

Takahashi

1993

The Journal of Physiology

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“…Although several papers report the critical role of proteoglycans in X. laevis development (17)(18)(19)(20)(21)(22), very limited information is available on GAG functions in amphibian embryogenesis (23)(24)(25). Therefore, we have characterized the X. laevis UGDH (xUGDH), the key enzyme in GAG biosynthesis in this model organism, as suitable for developmental studies.…”

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confidence: 99%

Molecular Cloning and Characterization of UDP-glucose Dehydrogenase from the Amphibian Xenopus laevis and Its Involvement in Hyaluronan Synthesis

Vigetti

Ori

Viola

et al. 2006

Journal of Biological Chemistry

111

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UDP-glucose dehydrogenase (UGDH) supplies the cell with UDP-glucuronic acid (UDP-GlcUA), a precursor of glycosaminoglycan and proteoglycan synthesis. Here we reported the cloning and the characterization of the UGDH from the amphibian Xenopus laevis that is one of the model organisms for developmental biology. We found that X. laevis UGDH (xUGDH) maintained a very high degree of similarity with other known UGDH sequences both at the genomic and the protein levels. Also its kinetic parameters are similar to those of UGDH from other species. During X. laevis development, UDGH is always expressed but clearly increases its mRNA levels at the tail bud stage (i.e. 30 h post-fertilization). This result fits well with our previous observation that hyaluronan, a glycosaminoglycan that is synthesized using UDP-GlcUA and UDP-N-acetylglucosamine, is abundantly detected at this developmental stage. The expression of UGDH was found to be related to hyaluronan synthesis. In human smooth muscle cells the overexpression of xUGDH or endogenous abrogation of UGDH modulated hyaluronan synthesis specifically. Our findings were confirmed by in vivo experiments where the silencing of xUGDH in X. laevis embryos decreased glycosaminoglycan synthesis causing severe embryonic malformations because of a defective gastrulation process.

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“…Neurocan doi: 10.7243/2055-4796-1-3 has been shown to bind FGFs and could be involved in their sequestration, local retention or presentation to target cells or their receptors [3,17]. Earlier studies had indicated the important role of extracellular matrix in the induction of neural-non-neural tissue in the early embryo [48]. In our present work, the abnormal expansion of neuroepithelium could have developed under the influence of the diffuse spread of FGF signals to adjacent cells.…”

Section: Discussionmentioning

confidence: 99%

Neurocan developmental expression and function during early avian embryogenesis

Georgadaki¹,

Zagris²

2014

Res J Dev Biol

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Background: Neurocan is the most abundant lectican considered to be expressed exclusively in the central nervous system. Neurocan interacts with other matrix components, with cell adhesion molecules, growth factors, enzymes and cell surface receptors. The interaction repertoire and evidence from cellular studies indicated an active role in signal transduction and major cellular programs. Relatively little is known about the neurocan tissue-specific distribution and function during embryonic development. This study examined the time of appearance and subsequent spatio-temporal expression pattern of neurocan and its functional activities during the earliest stages of development in the chick embryo. Methods: To detect the first expression and spatio-temporal distribution of neurocan in the early embryo, strand-specific reverse transcription-polymerase chain reaction (RT-PCR), immunoprecipitation and immunofluorescence were performed. An anti-neurocan blocking antibody transient pulse was applied to embryos at the onset of the neurula stage to perturb neurocan activities in the background of the current cellular signaling state of the developing embryo. Results: Neurocan was first detected in the inchoate neural plate and the extracellular matrix in embryos at the definitive streak stage (late gastrula). During early organogenesis, neurocan fluorescence was very intense in the neural tube, notochord, neural crest cells, pharyngeal arches, foregut lower wall, presumptive pronephric tubules, blood islands, dorsal mesocardium, intense in myocardium and distinct in endocardium, very intense in the presumptive cornea and intense in retina and lens, intense in somite and nephrotome. Antibody perturbation of neurocan function resulted in three predominant defects: (1) abnormal expansion of neuroepithelium in the surface ectoderm flanking the neural tube; (2) neural crest cells formed epithelial pockets located on the ectoderm apical surface; and (3) surface ectoderm cells (presumptive epidermis) acquired mesenchymal cell properties, invaded into the subectodermal space and interacted with neuroectoderm. Conclusions: Neurocan was first expressed in the inchoate neural plate at the late gastrula stage. Neurocan expression was very intense in the developing central nervous system as well as in many non-neural tissues. Neurocan seems to modulate signalling in the neural-non-neural tissue specification and the adhesive and signalling activities of epithelial-mesenchymal cells and neural crest cell motility in the early embryo.

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Extracellular matrix components prevent neural differentiation of disaggregated Xenopus ectoderm cells

Cited by 25 publications

References 28 publications

Neural differentiation in cleavage‐arrested ascidian blastomeres induced by a proteolytic enzyme.

Neural differentiation in cleavage‐arrested ascidian blastomeres induced by a proteolytic enzyme.

Molecular Cloning and Characterization of UDP-glucose Dehydrogenase from the Amphibian Xenopus laevis and Its Involvement in Hyaluronan Synthesis

Neurocan developmental expression and function during early avian embryogenesis

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