Faculty Opinions recommendation of Role of the isthmus and FGFs in resolving the paradox of neural crest plasticity and prepatterning.

Lamprey embryos were obtained by artificial fertilization to ascertain the contributions made by the neural crest to the head skeleton. Early-neurula-stage embryos of Petromyzon marinus were subjected to neural crest extirpation along the anterior half from one of seven zones, raised to a larval stage at which control larvae exhibit well-developed skeletons and analysed by light microscopy for any abnormalities to the cranial and visceral skeleton. The removal of premigratory neural crest at the level of the anterior prosencephalon (zone I) and at the level of somites 6 to 8 (zone VII) had no effect on skeletal development. However, the extirpation of neural crest from the intervening regions was positively correlated with deletions/reductions to the trabeculae (basicranial elements) and to the branchial arches (viscerocranial elements). Alterations to the trabeculae (16/27 cases, or 59%) occurred only after extirpation of zones II-V (corresponding to the posterior prosencephalon to midrhombencephalon) while alterations to the branchial arches (21/28 cases, or 75%) occurred only after removal of neural crest from zones III-VI (corresponding to the mesencephalon to the level of the fifth somite). Furthermore, the first three branchial arches were correlated in a majority of cases with neural crest from zone III, the next two arches with zones IV, V and VI and the last two arches with zone VI. Organs that develop within or adjacent to the area of neural crest extirpation such as the brain, notochord and lateral mesodermal derivatives were not affected. Parachordals were never altered by the operations nor were there any discernible changes to developing mucocartilage or to the prechondrogenic otic capsule. The contributions of the neural crest to the petromyzonid head skeleton described herein are compared with the roles of neural crest in the development of cranial and visceral skeletal elements in other vertebrates. The importance of these findings to the current hypothesis of the phylogeny of the vertebrate skeleton and the central role of the neural crest in vertebrate cephalization is discussed.

Download Full-text

Role of FGF signalling in neural crest cell migration during early chick embryo development

Zygote ◽

10.1017/s096719941800045x ◽

2018 ◽

Vol 26 (6) ◽

pp. 457-464 ◽

Cited By ~ 1

Author(s):

Xiao-tan Zhang ◽

Guang Wang ◽

Yan Li ◽

Manli Chuai ◽

Kenneth Ka Ho Lee ◽

...

Keyword(s):

Neural Crest ◽

Neural Tube ◽

Neural Crest Cell ◽

Dominant Negative ◽

Neural Tubes ◽

Dorsal Neural Tube ◽

Neural Crest Cell Migration ◽

Fgf Signalling ◽

Crest Cell

SummaryFibroblast growth factor (FGF) signalling acts as one of modulators that control neural crest cell (NCC) migration, but how this is achieved is still unclear. In this study, we investigated the effects of FGF signalling on NCC migration by blocking this process. Constructs that were capable of inducing Sprouty2 (Spry2) or dominant-negative FGFR1 (Dn-FGFR1) expression were transfected into the cells making up the neural tubes. Our results revealed that blocking FGF signalling at stage HH10 (neurulation stage) could enhance NCC migration at both the cranial and trunk levels in the developing embryos. It was established that FGF-mediated NCC migration was not due to altering the expression of N-cadherin in the neural tube. Instead, we determined that cyclin D1 was overexpressed in the cranial and trunk levels when Sprouty2 was upregulated in the dorsal neural tube. These results imply that the cell cycle was a target of FGF signalling through which it regulates NCC migration at the neurulation stage.

Download Full-text

Distribution of pluripotent neural crest cells in the embryo and the role of brain-derived neurotrophic factor in the commitment to the primary sensory neuron lineage

Journal of Neurobiology ◽

10.1002/neu.480240205 ◽

1993 ◽

Vol 24 (2) ◽

pp. 173-184 ◽

Cited By ~ 52

Author(s):

Maya Sieber-Blum ◽

Kazuo Ito ◽

Michael K. Richardson ◽

Carol J. Langtimm ◽

R. Scott Duff

Keyword(s):

Neural Crest ◽

Sensory Neuron ◽

Neurotrophic Factor ◽

Neural Crest Cells ◽

Brain Derived Neurotrophic Factor ◽

Primary Sensory Neuron

Download Full-text

Origins of the avian neural crest: the role of neural plate-epidermal interactions

Development ◽

10.1242/dev.121.2.525 ◽

1995 ◽

Vol 121 (2) ◽

pp. 525-538 ◽

Cited By ~ 39

Author(s):

M.A. Selleck ◽

M. Bronner-Fraser

Keyword(s):

Neural Crest ◽

Neural Crest Cell ◽

Neural Crest Cells ◽

Neural Plate ◽

Neural Tube Closure ◽

Whole Embryo Culture ◽

Early Stages ◽

Tissue Interactions ◽

Neural Ectoderm

We have investigated the lineage and tissue interactions that result in avian neural crest cell formation from the ectoderm. Presumptive neural plate was grafted adjacent to non-neural ectoderm in whole embryo culture to examine the role of tissue interactions in ontogeny of the neural crest. Our results show that juxtaposition of non-neural ectoderm and presumptive neural plate induces the formation of neural crest cells. Quail/chick recombinations demonstrate that both the prospective neural plate and the prospective epidermis can contribute to the neural crest. When similar neural plate/epidermal confrontations are performed in tissue culture to look at the formation of neural crest derivatives, juxtaposition of epidermis with either early (stages 4–5) or later (stages 6–10) neural plate results in the generation of both melanocytes and sympathoadrenal cells. Interestingly, neural plates isolated from early stages form no neural crest cells, whereas those isolated later give rise to melanocytes but not crest-derived sympathoadrenal cells. Single cell lineage analysis was performed to determine the time at which the neural crest lineage diverges from the epidermal lineage and to elucidate the timing of neural plate/epidermis interactions during normal development. Our results from stage 8 to 10+ embryos show that the neural plate/neural crest lineage segregates from the epidermis around the time of neural tube closure, suggesting that neural induction is still underway at open neural plate stages.

Download Full-text

Review: The Role of Wnt/β-Catenin Signalling in Neural Crest Development in Zebrafish

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.782445 ◽

2021 ◽

Vol 9 ◽

Author(s):

Gemma Sutton ◽

Robert N. Kelsh ◽

Steffen Scholpp

Keyword(s):

Neural Crest ◽

Pigment Cell ◽

Model Organism ◽

Neural Plate ◽

The Body ◽

Signalling Pathway ◽

Border Region ◽

Pigment Cells ◽

Neural Plate Border

The neural crest (NC) is a multipotent cell population in vertebrate embryos with extraordinary migratory capacity. The NC is crucial for vertebrate development and forms a myriad of cell derivatives throughout the body, including pigment cells, neuronal cells of the peripheral nervous system, cardiomyocytes and skeletogenic cells in craniofacial tissue. NC induction occurs at the end of gastrulation when the multipotent population of NC progenitors emerges in the ectodermal germ layer in the neural plate border region. In the process of NC fate specification, fate-specific markers are expressed in multipotent progenitors, which subsequently adopt a specific fate. Thus, NC cells delaminate from the neural plate border and migrate extensively throughout the embryo until they differentiate into various cell derivatives. Multiple signalling pathways regulate the processes of NC induction and specification. This review explores the ongoing role of the Wnt/β-catenin signalling pathway during NC development, focusing on research undertaken in the Teleost model organism, zebrafish (Danio rerio). We discuss the function of the Wnt/β-catenin signalling pathway in inducing the NC within the neural plate border and the specification of melanocytes from the NC. The current understanding of NC development suggests a continual role of Wnt/β-catenin signalling in activating and maintaining the gene regulatory network during NC induction and pigment cell specification. We relate this to emerging models and hypotheses on NC fate restriction. Finally, we highlight the ongoing challenges facing NC research, current gaps in knowledge, and this field’s potential future directions.

Download Full-text

Lineage-specific requirements of β-catenin in neural crest development

The Journal of Cell Biology ◽

10.1083/jcb.200209039 ◽

2002 ◽

Vol 159 (5) ◽

pp. 867-880 ◽

Cited By ~ 207

Author(s):

Lisette Hari ◽

Véronique Brault ◽

Maurice Kléber ◽

Hye-Youn Lee ◽

Fabian Ille ◽

...

Keyword(s):

Transcription Factor ◽

Neural Crest ◽

Neural Crest Cells ◽

Neural Crest Stem Cells ◽

Downstream Signaling ◽

Neural Crest Development ◽

Sensory Neurogenesis

β-Catenin plays a pivotal role in cadherin-mediated cell adhesion. Moreover, it is a downstream signaling component of Wnt that controls multiple developmental processes such as cell proliferation, apoptosis, and fate decisions. To study the role of β-catenin in neural crest development, we used the Cre/loxP system to ablate β-catenin specifically in neural crest stem cells. Although several neural crest–derived structures develop normally, mutant animals lack melanocytes and dorsal root ganglia (DRG). In vivo and in vitro analyses revealed that mutant neural crest cells emigrate but fail to generate an early wave of sensory neurogenesis that is normally marked by the transcription factor neurogenin (ngn) 2. This indicates a role of β-catenin in premigratory or early migratory neural crest and points to heterogeneity of neural crest cells at the earliest stages of crest development. In addition, migratory neural crest cells lateral to the neural tube do not aggregate to form DRG and are unable to produce a later wave of sensory neurogenesis usually marked by the transcription factor ngn1. We propose that the requirement of β-catenin for the specification of melanocytes and sensory neuronal lineages reflects roles of β-catenin both in Wnt signaling and in mediating cell–cell interactions.

Download Full-text