scholarly journals cdon and boc affect trunk neural crest cell migration through a non-cell autonomous reduction of hedgehog signaling in zebrafish slow-twitch muscle

2022 ◽  
Author(s):  
Ezra Lencer ◽  
Rytis Prekeris ◽  
Kristin Artinger
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Hedgehog Signaling ◽  
Neural Crest Cell ◽  
Vertebrate Development ◽  
Neural Crest Cell Migration ◽  
Slow Twitch Muscle ◽  
Slow Twitch ◽  
Neural Crest Migration ◽  
Crest Cell

The immunoglobin superfamily members cdon and boc are transmembrane proteins implicated in regulating hedgehog signaling during vertebrate development. Recent work showing roles for these genes in axon guidance and neural crest cell migration further suggest that cdon/boc may play additional functions in regulating directed cell movements during development. Here we use novel and existing mutants to investigate a role for cdon and boc in zebrafish neural crest cell migration. We find that single cdon or boc mutant embryos exhibit normal neural crest phenotypes, but that neural crest migration is strikingly disrupted in double cdon/boc mutant embryos. We further show that this neural crest migration phenotype is associated with defects to the differentiation of slow-twitch muscle cells, and that this slow-twitch muscle phenotype is a consequence of reduced hedgehog signaling in mutant fish. While neural crest migratory ability is not affected in double mutant embryos, neural crest directionality is severely affected. These data suggest that neural crest migration defects are likely to be secondary to defects in slow-twitch muscle differentiation. Combined, our data add to a growing literature showing that cdon and boc act synergistically to promote hedgehog signaling during vertebrate development, and provide a foundation for using zebrafish to further study the function of these hedgehog receptor paralogs.

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 rad21 Is Involved in Corneal Stroma Development by Regulating Neural Crest Migration

2020 ◽  
Vol 21 (20) ◽  
pp. 7807
Author(s):  
Bi Ning Zhang ◽  
Yu Liu ◽  
Qichen Yang ◽  
Pui Ying Leung ◽  
Chengdong Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Migration ◽  
Neural Crest ◽  
Corneal Stroma ◽  
Neural Crest Cell ◽  
Chromosome Conformation ◽  
Neural Crest Cell Migration ◽  
Neural Crest Migration ◽  
Crest Cell ◽  
Xenopus Laevis Embryos

Previously, we identified RAD21R450C from a peripheral sclerocornea pedigree. Injection of this rad21 variant mRNA into Xenopus laevis embryos disrupted the organization of corneal stroma fibrils. To understand the mechanisms of RAD21-mediated corneal stroma defects, gene expression and chromosome conformation analysis were performed using cells from family members affected by peripheral sclerocornea. Both gene expression and chromosome conformation of cell adhesion genes were affected in cells carrying the heterozygous rad21 variant. Since cell migration is essential in early embryonic development and sclerocornea is a congenital disease, we studied neural crest migration during cornea development in X. laevis embryos. In X. laevis embryos injected with rad21 mutant mRNA, neural crest migration was disrupted, and the number of neural crest-derived periocular mesenchymes decreased significantly in the corneal stroma region. Our data indicate that the RAD21R450C variant contributes to peripheral sclerocornea by modifying chromosome conformation and gene expression, therefore disturbing neural crest cell migration, which suggests RAD21 plays a key role in corneal stroma development.

scholarly journals Head Mesoderm Tissue Growth, Dynamics and Neural Crest Cell Migration

2019 ◽  
Author(s):  
Mary Cathleen McKinney ◽  
Rebecca McLennan ◽  
Rasa Giniunaite ◽  
Ruth E. Baker ◽  
Philip K. Maini ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Time Lapse ◽  
Tissue Growth ◽  
Dynamic Feedback ◽  
Head Mesoderm ◽  
Neural Crest Cell Migration ◽  
Neural Crest Migration ◽  
Crest Cell

ABSTRACTVertebrate head morphogenesis involves orchestrated cell growth and tissue movements of the mesoderm and neural crest to form the distinct craniofacial pattern. To better understand structural birth defects, it is important that we learn how these processes are controlled. Here, we examine this question during chick head morphogenesis using time-lapse imaging, computational modeling, and experiment. We find that head mesodermal cells are inherently dynamic in culture and alter cell behaviors in the presence of either ectoderm or neural crest cells. Mesodermal cells in vivo display large-scale whirling motions that rapidly transition to lateral, directed movements after neural crest cells emerge. Computer model simulations predict distinct changes in neural crest migration as the spatio-temporal growth profile of the mesoderm is varied. BrdU-labeling and photoconversion combined with cell density measurements then reveal non-uniform mesoderm growth in space and time. Chemical inhibition of head mesoderm proliferation or ablation of premigratory neural crest alters mesoderm growth and neural crest migration, implying a dynamic feedback between tissue growth and neural crest cell signaling to confer robustness to the system.Summary StatementDynamic feedback between tissue growth and neural crest cell migration ensures robust neural crest stream formation and head morphogenesis shown by time-lapse microscopy, mathematical modeling and embryo perturbations.

scholarly journals Proliferation dynamics associated with cranial neural crest cell migration

2011 ◽  
Vol 356 (1) ◽  
pp. 197
Author(s):  
Dennis A. Ridenour ◽  
Rebecca McLennan ◽  
Jessica M. Teddy ◽  
Katherine W. Prather ◽  
Craig L. Semerad ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Cranial Neural Crest ◽  
Cranial Neural Crest Cell ◽  
Neural Crest Cell Migration ◽  
Crest Cell

scholarly journals Timing of odontogenic neural crest cell migration and tooth-forming capability in mice

2003 ◽  
Vol 226 (4) ◽  
pp. 713-718 ◽  
Author(s):  
Yanding Zhang ◽  
Shusheng Wang ◽  
Yiqiang Song ◽  
Jun Han ◽  
Yang Chai ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cell Migration ◽  
Crest Cell

scholarly journals Foxc2 is required for proper cardiac neural crest cell migration, outflow tract septation, and ventricle expansion

2018 ◽  
Vol 247 (12) ◽  
pp. 1286-1296 ◽  
Author(s):  
Kimberly E. Inman ◽  
Carlo Donato Caiaffa ◽  
Kristin R. Melton ◽  
Lisa L. Sandell ◽  
Annita Achilleos ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Crest Cell ◽  
Outflow Tract ◽  
Cardiac Neural Crest ◽  
Neural Crest Cell Migration ◽  
Crest Cell

The distribution of fibronectin and tenascin along migratory pathways of the neural crest in the trunk of amphibian embryos

Development ◽  
1988 ◽  
Vol 103 (4) ◽  
pp. 743-756 ◽  
Author(s):  
H.H. Epperlein ◽  
W. Halfter ◽  
R.P. Tucker
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Pigment Cells ◽  
Dorsal Fin ◽  
Amphibian Embryos ◽  
Neural Crest Cell Migration ◽  
Crest Cell

It is generally assumed that in amphibian embryos neural crest cells migrate dorsally, where they form the mesenchyme of the dorsal fin, laterally (between somites and epidermis), where they give rise to pigment cells, and ventromedially (between somites and neural tube), where they form the elements of the peripheral nervous system. While there is agreement about the crest migratory routes in the axolotl (Ambystoma mexicanum), different opinions exist about the lateral pathway in Xenopus. We investigated neural crest cell migration in Xenopus (stages 23, 32, 35/36 and 41) using the X. laevis-X. borealis nuclear marker system and could not find evidence for cells migrating laterally. We have also used immunohistochemistry to study the distribution of the extracellular matrix (ECM) glycoproteins fibronectin (FN) and tenascin (TN), which have been implicated in directing neural crest cells during their migrations in avian and mammalian embryos, in the neural crest migratory pathways of Xenopus and the axolotl. In premigratory stages of the crest, both in Xenopus (stage 22) and the axolotl (stage 25), FN was found subepidermally and in extracellular spaces around the neural tube, notochord and somites. The staining was particularly intense in the dorsal part of the embryo, but it was also present along the visceral and parietal layers of the lateral plate mesoderm. TN, in contrast, was found only in the anterior trunk mesoderm in Xenopus; in the axolotl, it was absent. During neural crest cell migration in Xenopus (stages 25–33) and the axolotl (stages 28–35), anti-FN stained the ECM throughout the embryo, whereas anti-TN staining was limited to dorsal regions. There it was particularly intense medially, i.e. in the dorsal fin, around the neural tube, notochord, dorsal aorta and at the medial surface of the somites (stage 35 in both species). During postmigratory stages in Xenopus (stage 40), anti-FN staining was less intense than anti-TN staining. In culture, axolotl neural crest cells spread differently on FN- and TN-coated substrata. On TN, the onset of cellular outgrowth was delayed for about 1 day, but after 3 days the extent of outgrowth was indistinguishable from cultures grown on FN. However, neural crest cells in 3-day-old cultures were much more flattened on FN than on TN. We conclude that both FN and TN are present in the ECM that lines the neural crest migratory pathways of amphibian embryos at the time when the neural crest cells are actively migrating. FN is present in the embryonic ECM before the onset of neural crest migration.(ABSTRACT TRUNCATED AT 400 WORDS)

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