The Cell Biology of Neural Crest Cell Delamination and EMT

Taneyhill, Lisa A.; Padmanabhan, Rangarajan

doi:10.1016/b978-0-12-401730-6.00003-x

Cited by 6 publications

(5 citation statements)

References 176 publications

(150 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Initially, evidence from several model species indicated that NCCs undergo a "cadherin switch" from E-cadherin to N-cadherin during EMT. 131,132 Consistent with these findings, in zebrafish the premigratory NCCs predominantly express Ecadherin (Cdh1), whereas migratory NCCs predominantly express N-cadherin (Cdh2). 119,133 E-cadherin represses contact inhibition of locomotion (CIL) by controlling protrusions via Rac1 and p120.…”

Section: The Epithelial-to-mesenchymal Transitionsupporting

confidence: 60%

Neural crest development: insights from the zebrafish

Rocha

Singh

Ahsan

et al. 2019

Developmental Dynamics

View full text Add to dashboard Cite

Our understanding of the neural crest, a key vertebrate innovation, is built upon studies of multiple model organisms. Early research on neural crest cells (NCCs) was dominated by analyses of accessible amphibian and avian embryos, with mouse genetics providing complementary insights in more recent years. The zebrafish model is a relative newcomer to the field, yet it offers unparalleled advantages for the study of NCCs. Specifically, zebrafish provide powerful genetic and transgenic tools, coupled with rapidly developing transparent embryos that are ideal for high-resolution real-time imaging of the dynamic process of neural crest development. While the broad principles of neural crest development are largely conserved across vertebrate species, there are critical differences in anatomy, morphogenesis, and genetics that must be considered before information from one model is extrapolated to another. Here, our goal is to provide the reader with a helpful primer specific to neural crest development in the zebrafish model. We focus largely on the earliest events-specification, delamination, and migrationdiscussing what is known about zebrafish NCC development and how it differs from NCC development in non-teleost species, as well as highlighting current gaps in knowledge.

show abstract

Section: The Epithelial-to-mesenchymal Transitionsupporting

confidence: 60%

Neural crest development: insights from the zebrafish

Rocha

Singh

Ahsan

et al. 2019

Developmental Dynamics

View full text Add to dashboard Cite

show abstract

“…As a pseudo-stratified epithelium, the neural tube (and premigratory neural crest cells) possesses specific junctional complexes to maintain this epithelial state. These include both tight and adherens junctions ((Fishwick et al, 2012; Wu et al, 2011); reviewed in (Duband et al., 2015; Taneyhill and Schiffmacher, 2013)), along with the appropriate intracellular molecules, such as Rho family GTPases, that render these cells immotile (reviewed in (Kalcheim, 2015; Taneyhill and Padmanabhan, 2013)).…”

Section: A Formation Of the Neural Crestmentioning

confidence: 99%

Should I stay or should I go? Cadherin function and regulation in the neural crest

Taneyhill

Schiffmacher

2017

Genesis

Self Cite

View full text Add to dashboard Cite

Our increasing comprehension of neural crest cell development has reciprocally advanced our understanding of cadherin expression, regulation, and function. As a transient population of multipotent stem cells that significantly contribute to the vertebrate body plan, neural crest cells undergo a variety of transformative processes and exhibit many cellular behaviors, including epithelial-to-mesenchymal-transition (EMT), motility, collective cell migration, and differentiation. Multiple studies have elucidated regulatory and mechanistic details of specific cadherins during neural crest cell development in a highly contextual manner. Collectively, these results reveal that gradual changes within neural crest cells are accompanied by often times subtle, yet important, alterations in cadherin expression and function. The primary focus of this review is to coalesce recent data on cadherins in neural crest cells, from their specification to their emergence as motile cells soon after EMT, and to highlight the complexities of cadherin expression beyond our current perceptions, including the hypothesis that the neural crest EMT is a transition involving a predominantly singular cadherin switch. Further advancements in genetic approaches and molecular techniques will provide greater opportunities to integrate data from various model systems in order to distinguish unique or overlapping functions of cadherins expressed at any point throughout the ontogeny of the neural crest.

show abstract

“…Irrespective of which signaling pathways are involved, the formation of NCC involves tremendous cytoskeletal changes. During EMT, adjoining neuroepithelial cells lose their intracellular tight junctions, adherens junctions, and apicobasal polarity, and acquire focal adhesions, become polarized and migratory ( Taneyhill and Padmanabhan, 2014 ). These changes in cell adhesion are mediated in part by a “Cadherin switch” in which E-cadherin expression is downregulated in concert with N-cadherin upregulation ( Hatta and Takeichi, 1986 ; Coles et al, 2007 ).…”

Section: Neural Crest Cell and Craniofacial Developmentmentioning

confidence: 99%

Diabetes, Oxidative Stress, and DNA Damage Modulate Cranial Neural Crest Cell Development and the Phenotype Variability of Craniofacial Disorders

Fitriasari

Trainor

2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Craniofacial malformations are among the most common birth defects in humans and they often have significant detrimental functional, aesthetic, and social consequences. To date, more than 700 distinct craniofacial disorders have been described. However, the genetic, environmental, and developmental origins of most of these conditions remain to be determined. This gap in our knowledge is hampered in part by the tremendous phenotypic diversity evident in craniofacial syndromes but is also due to our limited understanding of the signals and mechanisms governing normal craniofacial development and variation. The principles of Mendelian inheritance have uncovered the etiology of relatively few complex craniofacial traits and consequently, the variability of craniofacial syndromes and phenotypes both within families and between families is often attributed to variable gene expression and incomplete penetrance. However, it is becoming increasingly apparent that phenotypic variation is often the result of combinatorial genetic and non-genetic factors. Major non-genetic factors include environmental effectors such as pregestational maternal diabetes, which is well-known to increase the risk of craniofacial birth defects. The hyperglycemia characteristic of diabetes causes oxidative stress which in turn can result in genotoxic stress, DNA damage, metabolic alterations, and subsequently perturbed embryogenesis. In this review we explore the importance of gene-environment associations involving diabetes, oxidative stress, and DNA damage during cranial neural crest cell development, which may underpin the phenotypic variability observed in specific craniofacial syndromes.

show abstract

The Cell Biology of Neural Crest Cell Delamination and EMT

Cited by 6 publications

References 176 publications

Neural crest development: insights from the zebrafish

Neural crest development: insights from the zebrafish

Should I stay or should I go? Cadherin function and regulation in the neural crest

Diabetes, Oxidative Stress, and DNA Damage Modulate Cranial Neural Crest Cell Development and the Phenotype Variability of Craniofacial Disorders

Contact Info

Product

Resources

About