Expression of tenascin in response to neural induction in amphibian embryos

Development ◽  
1988 ◽  
Vol 104 (3) ◽  
pp. 511-524 ◽  
Author(s):  
J.-F. Riou ◽  
D.-L. Shi ◽  
M. Chiquet ◽  
J.-C. Boucaut
Keyword(s):  
Cell Migration ◽  
Neural Crest Cell ◽  
Neural Induction ◽  
Gastrula Stage ◽  
Directed Cell Migration ◽  
Pleurodeles Waltl ◽  
Migration Pathways ◽  
Early Gastrula

The expression of tenascin, a constituent of extracellular matrix (ECM), was studied during the embryonic development of the amphibian Pleurodeles waltl. An antiserum to chick fibroblast tenascin was shown to cross-react with the homologous molecule of the amphibian. Immunostaining of embryo sections with anti-tenascin antiserum revealed that tenascin appears just after the completion of neurulation. At the tailbud stage, tenascin is present in the ECM located at sites of directed cell migration (neural crest cell migration pathways, extension of the pronephretic duct) and mesenchyme condensation (endocardium, aortic arches). The accumulation of tenascin immunoreactivity in the embryonic ECM is correlated with the synthesis of the 220×103Mr polypeptide of the molecule. To provide data on the patterning of tenascin, ectoderm and dorsal blastoporal lip isolated at early gastrula stage were cultured for a period of 3 days. Epidermal vesicles differentiating from isolated ectoderm completely lack tenascin. Conversely, axial mesoderm derivatives present in cultured dorsal blastoporal lip were found to produce tenascin. Neural induction of ectoderm isolated at early gastrula stage was performed in vitro with the dorsal blastoporal lip or concanavalin A. The induced neural tissue was found to accumulate tenascin. Spemann experiments confirmed in vivo that tenascin is expressed by ectodermal cells as a response to neural induction.

Expression of N-CAM precedes neural induction in Pleurodeles waltl (urodele, amphibian)

Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 675-683 ◽  
Author(s):  
J.P. Saint-Jeannet ◽  
F. Foulquier ◽  
C. Goridis ◽  
A.M. Duprat
Keyword(s):  
Monoclonal Antibody ◽  
Nervous System ◽  
Xenopus Laevis ◽  
Neural Induction ◽  
Gastrula Stage ◽  
Pleurodeles Waltl ◽  
Early Gastrula

The appearance and localization of N-CAM during neural induction were studied in Pleurodeles waltl embryos and compared with recent contradictory results reported in Xenopus laevis. A monoclonal antibody raised against mouse N-CAM was used. In the nervous system of Pleurodeles, it recognized two glycoproteins of 180 and 140×10(3) M(r) which are the Pleurodeles equivalent of N-CAM-180 and -140. Using this probe for immunohistochemistry and immunocytochemistry, we showed that N-CAM was already expressed in presumptive ectoderm at the early gastrula stage. In late gastrula embryos, a slight increase in staining was observed in the neurectoderm, whereas the labelling persisted in the noninduced ectoderm. When induced ectodermal cells were isolated at the late gastrula stage and cultured in vitro up to 14 days, a faint polarized labelling of cells was observed initially. During differentiation, the staining increased and became progressively restricted to differentiating neurons.

Initiation of mesodermal cell migration and spreading relative to gastrulation in the urodele amphibian Pleurodeles waltl

Development ◽  
1989 ◽  
Vol 105 (2) ◽  
pp. 351-363 ◽  
Author(s):  
D.-L. Shi ◽  
T. Darribere ◽  
K.E. Johnson ◽  
J.-C. Boucaut
Keyword(s):  
Cell Migration ◽  
Marginal Zone ◽  
Gastrula Stage ◽  
Cell Stage ◽  
Animal Pole ◽  
Mesodermal Cell ◽  
Marginal Cells ◽  
Pleurodeles Waltl ◽  
Early Gastrula

We have investigated the autonomous migration of marginal cells and their interactions with extracellular matrix (ECM) located on the inner surface of the blastocoel roof in the urodele amphibian, Pleurodeles waltl, using a novel in vitro migration assay. Animal hemispheres containing equatorial cells removed at different cleavage stages and dorsal marginal zone (DMZ) explants of early gastrula stage were cultured either on fibronectin (FN)-coated or ECM-conditioned substrata. In explanted animal hemispheres, dorsal marginal cells showed autonomous migration on FN-coated substratum at the same time as the onset of gastrulation in control embryos. They acquired this capacity at least at the 32-cell stage, whereas lateral and ventral marginal cells acquired it after the 64-cell stage. DMZ outgrowths of early gastrula stage exhibited autonomous spreading on both substrata. In addition, we showed that they spread preferentially toward the animal pole when deposited on substratum conditioned by the dorsal roof of the blastocoel. By culturing dissociated marginal cells on ECM- conditioned substratum, we also found that increased spreading capacity of marginal cells was related to the initiation of their migration. A comparative study of the migration of marginal cells in ultraviolet (u.v.)-irradiated and normal embryos was also made. The results indicate that dorsal marginal cell migration was absent or dramatically reduced by u.v.-irradiation. These results suggest that the differential acquisition in the spreading capacity both in timing and in intensity around the marginal zone was correlated with the sequential involution of mesodermal cells in the course of gastrulation.

scholarly journals Lamellipodin and the Scar/WAVE complex cooperate to promote cell migration in vivo

2013 ◽  
Vol 203 (4) ◽  
pp. 673-689 ◽  
Author(s):  
Ah-Lai Law ◽  
Anne Vehlow ◽  
Maria Kotini ◽  
Lauren Dodgson ◽  
Daniel Soong ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Direct Interaction ◽  
Dependent Manner ◽  
Border Cell ◽  
Promote Cell Migration ◽  
Wave Complex

Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism. Here, we report that Lpd directly binds active Rac, which regulates a direct interaction between Lpd and the Scar/WAVE complex via Abi. Consequently, Lpd controls lamellipodium size, cell migration speed, and persistence via Scar/WAVE in vitro. Moreover, Lpd knockout mice display defective pigmentation because fewer migrating neural crest-derived melanoblasts reach their target during development. Consistently, Lpd regulates mesenchymal neural crest cell migration cell autonomously in Xenopus laevis via the Scar/WAVE complex. Further, Lpd’s Drosophila melanogaster orthologue Pico binds Scar, and both regulate collective epithelial border cell migration. Pico also controls directed cell protrusions of border cell clusters in a Scar-dependent manner. Taken together, Lpd is an essential, evolutionary conserved regulator of the Scar/WAVE complex during cell migration in vivo.

Evidence for collapsin-1 functioning in the control of neural crest migration in both trunk and hindbrain regions

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2181-2189 ◽  
Author(s):  
B.J. Eickholt ◽  
S.L. Mackenzie ◽  
A. Graham ◽  
F.S. Walsh ◽  
P. Doherty
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Axon Growth ◽  
Neural Crest Cells ◽  
Neural Crest Cell Migration ◽  
Neural Crest Migration ◽  
Migration Pathways ◽  
Crest Cell

Collapsin-1 belongs to the Semaphorin family of molecules, several members of which have been implicated in the co-ordination of axon growth and guidance. Collapsin-1 can function as a selective chemorepellent for sensory neurons, however, its early expression within the somites and the cranial neural tube (Shepherd, I., Luo, Y., Raper, J. A. and Chang, S. (1996) Dev. Biol. 173, 185–199) suggest that it might contribute to the control of additional developmental processes in the chick. We now report a detailed study on the expression of collapsin-1 as well as on the distribution of collapsin-1-binding sites in regions where neural crest cell migration occurs. collapsin-1 expression is detected in regions bordering neural crest migration pathways in both the trunk and hindbrain regions and a receptor for collapsin-1, neuropilin-1, is expressed by migrating crest cells derived from both regions. When added to crest cells in vitro, a collapsin-1-Fc chimeric protein induces morphological changes similar to those seen in neuronal growth cones. In order to test the function of collapsin-1 on the migration of neural crest cells, an in vitro assay was used in which collapsin-1-Fc was immobilised in alternating stripes consisting of collapsin-Fc/fibronectin versus fibronectin alone. Explanted neural crest cells derived from both trunk and hindbrain regions avoided the collapsin-Fc-containing substratum. These results suggest that collapsin-1 signalling can contribute to the patterning of neural crest cell migration in the developing chick.

scholarly journals Cortactin Promotes Migration and Platelet-derived Growth Factor-induced Actin Reorganization by Signaling to Rho-GTPases

2009 ◽  
Vol 20 (14) ◽  
pp. 3209-3223 ◽  
Author(s):  
Frank P.L. Lai ◽  
Malgorzata Szczodrak ◽  
J. Margit Oelkers ◽  
Markus Ladwein ◽  
Filippo Acconcia ◽  
...  
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Rho Gtpases ◽  
Platelet Derived Growth Factor ◽  
Actin Assembly ◽  
Actin Reorganization ◽  
Directed Cell Migration ◽  
Syndrome Protein

Dynamic actin rearrangements are initiated and maintained by actin filament nucleators, including the Arp2/3-complex. This protein assembly is activated in vitro by distinct nucleation-promoting factors such as Wiskott-Aldrich syndrome protein/Scar family proteins or cortactin, but the relative in vivo functions of each of them remain controversial. Here, we report the conditional genetic disruption of murine cortactin, implicated previously in dynamic actin reorganizations driving lamellipodium protrusion and endocytosis. Unexpectedly, cortactin-deficient cells showed little changes in overall cell morphology and growth. Ultrastructural analyses and live-cell imaging studies revealed unimpaired lamellipodial architecture, Rac-induced protrusion, and actin network turnover, although actin assembly rates in the lamellipodium were modestly increased. In contrast, platelet-derived growth factor-induced actin reorganization and Rac activation were impaired in cortactin null cells. In addition, cortactin deficiency caused reduction of Cdc42 activity and defects in random and directed cell migration. Reduced migration of cortactin null cells could be restored, at least in part, by active Rac and Cdc42 variants. Finally, cortactin removal did not affect the efficiency of receptor-mediated endocytosis. Together, we conclude that cortactin is fully dispensable for Arp2/3-complex activation during lamellipodia protrusion or clathrin pit endocytosis. Furthermore, we propose that cortactin promotes cell migration indirectly, through contributing to activation of selected Rho-GTPases.

scholarly journals DAN (NBL1) promotes collective neural crest migration by restraining uncontrolled invasion

2017 ◽  
Vol 216 (10) ◽  
pp. 3339-3354 ◽  
Author(s):  
Rebecca McLennan ◽  
Caleb M. Bailey ◽  
Linus J. Schumacher ◽  
Jessica M. Teddy ◽  
Jason A. Morrison ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Metastatic Melanoma ◽  
Neural Crest Cell ◽  
Bmp Signaling ◽  
Loss Of Function ◽  
Neural Crest Cell Migration ◽  
Crest Cell

Neural crest cells are both highly migratory and significant to vertebrate organogenesis. However, the signals that regulate neural crest cell migration remain unclear. In this study, we test the function of differential screening-selected gene aberrant in neuroblastoma (DAN), a bone morphogenetic protein (BMP) antagonist we detected by analysis of the chick cranial mesoderm. Our analysis shows that, before neural crest cell exit from the hindbrain, DAN is expressed in the mesoderm, and then it becomes absent along cell migratory pathways. Cranial neural crest and metastatic melanoma cells avoid DAN protein stripes in vitro. Addition of DAN reduces the speed of migrating cells in vivo and in vitro, respectively. In vivo loss of function of DAN results in enhanced neural crest cell migration by increasing speed and directionality. Computer model simulations support the hypothesis that DAN restrains cell migration by regulating cell speed. Collectively, our results identify DAN as a novel factor that inhibits uncontrolled neural crest and metastatic melanoma invasion and promotes collective migration in a manner consistent with the inhibition of BMP signaling.

scholarly journals In vivo Neural Crest Cell Migration Is Controlled by “Mixotaxis”

2020 ◽  
Vol 11 ◽  
Author(s):  
Elias H. Barriga ◽  
Eric Theveneau
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Electric Fields ◽  
Cellular Response ◽  
Cancer Metastasis ◽  
Neural Crest Cell ◽  
Cell Types ◽  
Directed Cell Migration ◽  
Hard Truth

Directed cell migration is essential all along an individual’s life, from embryogenesis to tissue repair and cancer metastasis. Thus, due to its biomedical relevance, directed cell migration is currently under intense research. Directed cell migration has been shown to be driven by an assortment of external biasing cues, ranging from gradients of soluble (chemotaxis) to bound (haptotaxis) molecules. In addition to molecular gradients, gradients of mechanical properties (duro/mechanotaxis), electric fields (electro/galvanotaxis) as well as iterative biases in the environment topology (ratchetaxis) have been shown to be able to direct cell migration. Since cells migrating in vivo are exposed to a challenging environment composed of a convolution of biochemical, biophysical, and topological cues, it is highly unlikely that cell migration would be guided by an individual type of “taxis.” This is especially true since numerous molecular players involved in the cellular response to these biasing cues are often recycled, serving as sensor or transducer of both biochemical and biophysical signals. In this review, we confront literature on Xenopus cephalic neural crest cells with that of other cell types to discuss the relevance of the current categorization of cell guidance strategies. Furthermore, we emphasize that while studying individual biasing signals is informative, the hard truth is that cells migrate by performing a sort of “mixotaxis,” where they integrate and coordinate multiple inputs through shared molecular effectors to ensure robustness of directed cell motion.

scholarly journals Collagens in avian neural crest development: distribution in vivo and migration-promoting ability in vitro

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 969-984 ◽  
Author(s):  
R. Perris ◽  
D. Krotoski ◽  
M. Bronner-Fraser
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Cell Movement ◽  
Neural Crest Cell ◽  
Basement Membranes ◽  
Neural Crest Development ◽  
Neural Crest Cell Migration ◽  
Crest Cell

This study examines the spatiotemporal distribution of collagen (Col) types I-V and IX during neural crest development in vivo and their ability to support neural crest cell movement in vitro. Col I, III and IV were widespread throughout the embryo, including the neural crest migratory pathways, whereas Col II, V and IX preferentially localized to regions from which migrating neural crest cells were absent. Col I-IV and IX occurred both in association with basement membranes and within interstitial matrices, whereas Col V only was detected in juxtaposition to basement membranes. Although initially distributed throughout the rostrocaudal extent of the somitic sclerotome, Col I and III rearranged to the caudal portion with progressive neural crest cell migration through the rostral portion of the sclerotome. This rearrangement does not occur in neural crest-ablated embryos, suggesting that it is a direct consequence of neural crest cell migration. The perinotochordal matrix, avoided by neural crest cells, contained a metameric Col II/IX immunoreactivity along the rostrocaudal axis which alternated with that of Col I and III. In contrast, Col IV and V were not observed in this matrix, but lined the basement membranes of the notochord and ventrolateral neural tube. To determine their functional significance for neural crest cell migration in vivo, purified collagens were tested for their ability to promote neural crest cell motility in vitro. Neural crest cell migration on isolated collagens was most pronounced on Col I and IV, whereas Col II, V and the triple-helical fragment of Col VII were unable to support cell motility. Substrata created by copolymerization of Col I and fibronectin, or Col I and laminin-nidogen, supported cell motility better than Col I alone, whereas both Col V and a cartilage-type chondroitin sulfate proteoglycan reduced cell movement on Col I. Fibronectin bound to pre-immobilized monomeric Col I, II or V had a reduced ability to support neural crest cell movement when compared to fibronectin alone. A similar reduction was seen for Col IV bound to the low density heparan sulfate proteoglycan from the EHS mouse tumor. The results demonstrate that Col I-IX are differentially distributed in the early avian embryo. During neural crest development several of these collagens undergo dynamic reorganizations that correlate with the migration of neural crest cells. Furthermore, various collagens possess distinct abilities to support neural crest cell migration in vitro, and their migration-promoting activity can be modulated by their conformation and/or association with other matrix components.

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