The development, patterning and evolution of neural crest cell differentiation into cartilage and bone

Dash, Soma; Trainor, Paul A.

doi:10.1016/j.bone.2020.115409

Cited by 77 publications

(69 citation statements)

References 191 publications

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“…The distribution of the neural crest in the midgestation embryo includes several discrete accumulations of mesenchymal cells at bilaterally symmetrical locations ( Figures 1B,C, 2). The neural crest-derived mesenchyme at some of these sites will contribute to special sensory organs: the frontonasal masses [olfactory epithelium (OE) and nose], the eyes (cornea, scleral, and choroidal cells), and the otic placodes (middle ear bones and epithelia); others will generate cranial skeletal elements, teeth, and cartilage (Jiang et al, 2002;Lwigale et al, 2004;Tucker and Sharpe, 2004;Balmer and LaMantia, 2005;Creuzet et al, 2005;Yoshida et al, 2008;Edlund et al, 2015;Williams and Bohnsack, 2015;Dash and Trainor, 2020). Each of these mesenchymal neural crest populations derives from a distinct anterior to posterior (A-P) location in the mesencephalic, rhombencephalic, vagal/cardiac, or trunk neural crest ( Figure 1B).…”

Section: Introductionmentioning

confidence: 99%

“…This requirement for adaptive flexibility to match the face and the brain with environment and niche may be solved by deploying neural crest cells, in varying quantities with modest changes in molecular identities and genetic control networks (Depew et al, 2005;Yu, 2010;Moody and LaMantia, 2015). Once in place, similarly modest variations of neural crest/placode M/E interaction, signaling pathways, and downstream transcriptional regulation (Cotney et al, 2013;Graf et al, 2016;Dubey et al, 2018;Williams and Bohnsack, 2019;Dash and Trainor, 2020) could result in species-specific distinctions in register with demands of adaptation and selection. Such flexibility in individuals or species for neural crest as inductive ambassadors would yield substantial adaptive capacity.…”

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confidence: 99%

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Why Does the Face Predict the Brain? Neural Crest Induction, Craniofacial Morphogenesis, and Neural Circuit Development

LaMantia

2020

Front. Physiol.

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Mesenchephalic and rhombencephalic neural crest cells generate the craniofacial skeleton, special sensory organs, and subsets of cranial sensory receptor neurons. They do so while preserving the anterior-posterior (A-P) identity of their neural tube origins. This organizational principle is paralleled by central nervous system circuits that receive and process information from facial structures whose A-P identity is in register with that in the brain. Prior to morphogenesis of the face and its circuits, however, neural crest cells act as “inductive ambassadors” from distinct regions of the neural tube to induce differentiation of target craniofacial domains and establish an initial interface between the brain and face. At every site of bilateral, non-axial secondary induction, neural crest constitutes all or some of the mesenchymal compartment for non-axial mesenchymal/epithelial (M/E) interactions. Thus, for epithelial domains in the craniofacial primordia, aortic arches, limbs, the spinal cord, and the forebrain (Fb), neural crest-derived mesenchymal cells establish local sources of inductive signaling molecules that drive morphogenesis and cellular differentiation. This common mechanism for building brains, faces, limbs, and hearts, A-P axis specified, neural crest-mediated M/E induction, coordinates differentiation of distal structures, peripheral neurons that provide their sensory or autonomic innervation in some cases, and central neural circuits that regulate their behavioral functions. The essential role of this neural crest-mediated mechanism identifies it as a prime target for pathogenesis in a broad range of neurodevelopmental disorders. Thus, the face and the brain “predict” one another, and this mutual developmental relationship provides a key target for disruption by developmental pathology.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

Why Does the Face Predict the Brain? Neural Crest Induction, Craniofacial Morphogenesis, and Neural Circuit Development

LaMantia

2020

Front. Physiol.

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“…At E11.5, LacZ staining was observed in the nasal process and the pharyngeal arches ( Figure 6B), structures populated by cephalic neural crest cells (NCCs) that will contribute to form the skull and facial skeleton. 43,44 At E11.5, LacZ staining was also detected in mesodermal derivatives including the ventro-medial cells of the somites ( Figure 6C), which will also undergo epithelial-tomesenchymal transition (EMT) to form the sclerotomes which will, in turn, give rise to the vertebrae and the ribs. In addition, staining was detected in the lung bud ( Figure 6C), as previously reported 22 and in Rathke's pouch, a structure deriving from the oral ectoderm which will give rise to the adenohypophysis of the pituitary gland.…”

Section: Sned1 Is Expressed In Skeletal and Craniofacial Precursorsmentioning

confidence: 99%

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Barqué

Jan

Fuente

et al. 2018

Preprint

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AbstractBackgroundThe extracellular matrix (ECM) is a fundamental component of multicellular organisms that orchestrates developmental processes and controls cell and tissue organization. We previously identified the novel ECM protein SNED1 as a promoter of breast cancer metastasis and showed that its level of expression negatively correlated with survival of breast cancer patients. Here we sought to identify the roles of SNED1 during murine development and in physiology.ResultsWe generated two novel Sned1 knockout mouse strains and showed that Sned1 is essential since homozygous ablation of the gene led to ~67% early neonatal lethality. Phenotypic analysis of the surviving knockout mice obtained revealed a role for SNED1 in the development of craniofacial and skeletal structures since Sned1 knockout resulted in growth defects, nasal cavity occlusion, and craniofacial malformations. Sned1 is widely expressed in embryos, notably in neural-crest derivatives. We further show here that mice with a neural-crest-cell-specific deletion of Sned1 survive, but display facial anomalies partly phenocopying the global knockout mice.ConclusionsOur results demonstrate requisite roles for SNED1 during development and neonatal survival. Importantly, the deletion of 2q37.3 in humans, a region that includes the SNED1 locus, has been associated with facial dysmorphism and short stature.

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“…Bone and cartilage are important structures which forms the framework of the body, supporting, protecting and moving the body. Bones in different parts of the skeleton develop through two distinct processes [1], intramembranous ossification and intracartilaginous ossification. In intramebranous ossification, bones ossify directly without passing from the connective tissue structure to the cartilage tissue.…”

Section: Introductionmentioning

confidence: 99%

Age-related histological changes in rat tibia

Chen

Tan

et al. 2021

Folia Morphol

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The development, patterning and evolution of neural crest cell differentiation into cartilage and bone

Cited by 77 publications

References 191 publications

Why Does the Face Predict the Brain? Neural Crest Induction, Craniofacial Morphogenesis, and Neural Circuit Development

Why Does the Face Predict the Brain? Neural Crest Induction, Craniofacial Morphogenesis, and Neural Circuit Development

Knockout of the gene encoding the extracellular matrix protein SNED1 results in early neonatal lethality and craniofacial malformations

Age-related histological changes in rat tibia

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