7 Neural Crest Diversification

Groves, Andrew K.; Bronner‐Fraser, Marianne

doi:10.1016/s0070-2153(08)60383-x

Cited by 46 publications

(25 citation statements)

References 266 publications

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“…A third population of ectodermal cells, the neural crest, form either as the neural folds are elevating and converging (e.g., in the mouse) or during their fusion (e.g., in the chick). The neural crest is an important cell type that contributes extensively to the peripheral nervous system, among other structures (e.g., pigment cells, facial skeleton) reviewed by Anderson, 1999;GarciaCastro and Bronner-Fraser, 1999;Groves and Bronner-Fraser, 1999;Hall, 1999;Le Douarin and Kalcheim, 1999).…”

Section: Closure Of the Neural Groovementioning

confidence: 99%

Towards a cellular and molecular understanding of neurulation

Colas

Schoenwolf

2001

Developmental Dynamics

399

376

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Neurulation occurs during the early embryogenesis of chordates, and it results in the formation of the neural tube, a dorsal hollow nerve cord that constitutes the rudiment of the entire adult central nervous system. The goal of studies on neurulation is to understand its tissue, cellular and molecular basis, as well as how neurulation is perturbed during the formation of neural tube defects. The tissue basis of neurulation consists of a series of coordinated morphogenetic movements within the primitive streak (e.g., regression of Hensen's node) and nascent primary germ layers formed during gastrulation. Signaling occurs between Hensen's node and the nascent ectoderm, initiating neurulation by inducing the neural plate (i.e., actually, by suppressing development of the epidermal ectoderm). Tissue movements subsequently result in shaping and bending of the neural plate and closure of the neural groove. The cellular basis of the tissue movements of neurulation consists of changes in the behavior of the constituent cells; namely, changes in cell number, position, shape, size and adhesion. Neurulation, like any morphogenetic event, occurs within the milieu of generic biophysical determinants of form present in all living tissues. Such forces govern and to some degree control morphogenesis in a tissue-autonomous manner. The molecular basis of neurulation remains largely unknown, but we suggest that neurulation genes have evolved to work in concert with such determinants, so that appropriate changes occur in the behaviors of the correct populations of cells at the correct time, maximizing the efficiency of neurulation and leading to heritable speciesand axial-differences in this process. In this article, we review the tissue and cellular basis of neurulation and provide strategies to determine its molecular basis. We expect that such strategies will lead to the identification in the near future of critical neurulation genes, genes that when mutated perturb neurulation in a highly specific and predictable fashion and cause neurulation defects, thereby contributing to the formation of neural tube defects.

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Section: Closure Of the Neural Groovementioning

confidence: 99%

Towards a cellular and molecular understanding of neurulation

Colas

Schoenwolf

2001

Developmental Dynamics

399

376

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“…The reader is referred to additional reviews that focus on later stages of development which deal with cell migration, phenotypic diversification and differentiation (Anderson, 1999;Christiansen et al, 2000;Groves andBronner-Fraser, 1999, Kalcheim, 2000). The discovery of genes that identify prospective neural crest cells still resident in the neuroepithelium made it possible to address the cellular and molecular events that underly the formation of this cell type (see section III).…”

Section: General Introductionmentioning

confidence: 99%

Early stages of neural crest ontogeny: formation and regulation of cell delamination

Kalcheim

Burstyn‐Cohen²

2005

Int. J. Dev. Biol.

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Long standing research of the Neural Crest embodies the most fundamental questions of Developmental Biology. Understanding the mechanisms responsible for specification, delamination, migration and phenotypic differentiation of this highly diversifying group of progenitors has been a challenge for many researchers over the years and continues to attract newcomers into the field. Only a few leaps were more significant than the discovery and successful exploitation of the quail-chick model by Nicole Le Douarin and colleagues from the Institute of Embryology at Nogent-sur-Marne. The accurate fate mapping of the neural crest performed at virtually all axial levels was followed by the determination of its developmental potentialities as initially analysed at a population level and then followed by many other significant findings. Altogether, these results paved the way to innumerable questions which brought us from an organismic view to mechanistic approaches. Among them, elucidation of functions played by identified genes is now rapidly underway. Emerging results lead the way back to an integrated understanding of the nature of interactions between the developing neural crest and neighbouring structures. The Nogent Institute thus performed an authentic «tour de force» in bringing the Neural Crest to the forefront of Developmental Biology. The present review is dedicated to the pivotal contributions of Nicole Le Douarin and her collaborators and to unforgettable memories that one of the authors bears from the time spent in the Nogent Institute. We summarize here recent advances in our understanding of early stages of crest ontogeny that comprise specification of epithelial progenitors to a neural crest fate and the onset of neural crest migration. Particular emphasis is given to signaling by BMP and Wnt molecules, to the role of the cell cycle in generating cell movement and to possible interactions between both mechanisms.

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“…This process yields mature neurons that express a limited set of genes encoding proteins that perform specific functions (1)(2)(3)(4)(5)(6)(7)(8)(9). Part of this repertoire of genes is that of encoding proteins required for neuronal signaling, including neurotransmitter biosynthetic enzymes and their cognate neurotransmitter receptors.…”

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confidence: 99%

Transcriptional Repression by a Conserved Intronic Sequence in the Nicotinic Receptor α3 Subunit Gene

Medel

Gardner

2007

Journal of Biological Chemistry

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The genes encoding the nicotinic acetylcholine receptor ␣3, ␣5, and ␤4 subunits are genomically clustered. These genes are co-expressed in a variety of cells in the peripheral and central nervous systems. Their gene products assemble in a number of stoichiometries to generate several nicotinic receptor subtypes that have distinct pharmacological and physiological properties. Signaling through these receptors is critical for a variety of fundamental biological processes. Despite their importance, the transcriptional mechanisms underlying their coordinated expression remain to be completely elucidated. By using a bioinformatics approach, we identified a highly conserved intronic sequence within the fifth intron of the ␣3 subunit gene. Reporter gene analysis demonstrated that this sequence, termed "␣3 intron 5," inhibits the transcriptional activities of the ␣3 and ␤4 subunit gene promoters. This repressive activity is position-and orientation-independent. Importantly, repression occurs in a cell type-specific manner, being present in cells that do not express the receptor genes or expresses them at very low levels. Electrophoretic mobility shift assays demonstrate that nuclear proteins specifically interact with ␣3 intron 5 at two distinct sites. We propose that this intronic repressor element is important for the restricted expression patterns of the nicotinic receptor ␣3 and ␤4 subunit genes.Neuronal differentiation is a consequence of extrinsic and intrinsic regulatory cascades that ultimately act to regulate, both positively and negatively, gene expression. This process yields mature neurons that express a limited set of genes encoding proteins that perform specific functions (1-9). Part of this repertoire of genes is that of encoding proteins required for neuronal signaling, including neurotransmitter biosynthetic enzymes and their cognate neurotransmitter receptors. Acetylcholine is an excitatory neurotransmitter that interacts with both ionotropic and G-protein-coupled receptors. Signaling through ionotropic nicotinic acetylcholine (nACh) 2 receptors is involved in a variety of behaviors ranging from muscle contraction to memory formation (10 -13). In addition, acetylcholine and its receptors play important roles in neural development (14 -17). Not surprisingly, compromised signaling through nACh receptors is implicated in a number of neurological disorders (18 -35). Thus, understanding the molecular details underlying nACh receptor expression will shed light on various aspects of neural development and function as well as contribute to our understanding of several neuropathological conditions.In the nervous system, nACh receptors are encoded by a conserved family of genes consisting of at least 12 members, ␣2-␣10 and ␤2-␤4 (10, 11, 36 -39). A significant effort has been put forth to elucidate transcriptional mechanisms controlling expression of the nACh receptor genes (40, 41). We and others have focused on the regulation of a genomic cluster of receptor genes, those encoding the ␣3, ␣5, and ␤4 subunits (4...

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7 Neural Crest Diversification

Cited by 46 publications

References 266 publications

Towards a cellular and molecular understanding of neurulation

Towards a cellular and molecular understanding of neurulation

Early stages of neural crest ontogeny: formation and regulation of cell delamination

Transcriptional Repression by a Conserved Intronic Sequence in the Nicotinic Receptor α3 Subunit Gene

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