scholarly journals The lamprey: A jawless vertebrate model system for examining origin of the neural crest and other vertebrate traits

2014 ◽  
Vol 87 (1-2) ◽  
pp. 44-51 ◽  
Author(s):  
Stephen A. Green ◽  
Marianne E. Bronner
Keyword(s):  
Neural Crest ◽  
Model System ◽  
Jawless Vertebrate ◽  
Vertebrate Model

scholarly journals Hematopoietic and neural crest defects in zebrafishshoc2mutants: a novel vertebrate model for Noonan-like syndrome

2018 ◽  
Vol 28 (3) ◽  
pp. 501-514 ◽  
Author(s):  
HyeIn Jang ◽  
Erin Oakley ◽  
Marie Forbes-Osborne ◽  
Melissa V Kesler ◽  
Rebecca Norcross ◽  
...  
Keyword(s):  
Neural Crest ◽  
Vertebrate Model

scholarly journals 16p12.1 deletion orthologs are expressed in motile neural crest cells and are important for regulating craniofacial development in Xenopus laevis

2020 ◽  
Author(s):  
Micaela Lasser ◽  
Jessica Bolduc ◽  
Luke Murphy ◽  
Caroline O'Brien ◽  
Sangmook Lee ◽  
...  
Keyword(s):  
Xenopus Laevis ◽  
Neural Crest ◽  
Expression Patterns ◽  
Copy Number Variants ◽  
Neural Crest Cell ◽  
Underlying Mechanism ◽  
Craniofacial Development ◽  
Pharyngeal Arches ◽  
Individual Gene ◽  
Vertebrate Model

Copy number variants (CNVs) associated with neurodevelopmental disorders are characterized by extensive phenotypic heterogeneity. In particular, one CNV was identified in a subset of children clinically diagnosed with intellectual disabilities (ID) that results in a hemizygous deletion of multiple genes at chromosome 16p12.1. In addition to ID, individuals with this deletion display a variety of symptoms including microcephaly, seizures, cardiac defects, and growth retardation. Moreover, patients also manifest severe craniofacial abnormalities, such as micrognathia, cartilage malformation of the ears and nose, and facial asymmetries; however, the function of the genes within the 16p12.1 region have not been studied in the context of vertebrate craniofacial development. The craniofacial tissues affected in patients with this deletion all derive from the same embryonic precursor, the cranial neural crest, leading to the hypothesis that one or more of the 16p12.1 genes may be involved in regulating neural crest cell (NCC)-related processes. To examine this, we characterized the developmental role of the 16p12.1-affected gene orthologs, polr3e, mosmo, uqcrc2, and cdr2, during craniofacial morphogenesis in the vertebrate model system, Xenopus laevis. While the currently-known cellular functions of these genes are diverse, we find that they share similar expression patterns along the neural tube, pharyngeal arches, and later craniofacial structures. As these genes show co-expression in the pharyngeal arches where NCCs reside, we sought to elucidate the effect of individual gene depletion on craniofacial development and NCC migration. We find that reduction of several 16p12.1 genes significantly disrupts craniofacial and cartilage formation, pharyngeal arch migration, as well as NCC specification and motility. Thus, we have determined that some of these genes play an essential role during vertebrate craniofacial patterning by regulating specific processes during NCC development, which may be an underlying mechanism contributing to the craniofacial defects associated with the 16p12.1 deletion.

scholarly journals The embryonic neural crest microenvironment as a model system to explore tumor cell reprogramming and metastatic ability

2007 ◽  
Vol 306 (1) ◽  
pp. 369 ◽  
Author(s):  
Paul M. Kulesa ◽  
Jennifer C. Kasemeier ◽  
Jessica M. Teddy ◽  
Naira V. Margaryan ◽  
Elisabeth A. Seftor ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Neural Crest ◽  
Model System ◽  
Cell Reprogramming

scholarly journals Understanding neural crest cell development using Gcnf−/− mutant mice as a model system

2011 ◽  
Vol 356 (1) ◽  
pp. 185
Author(s):  
Annita Achilleos ◽  
Jennie Crane ◽  
Shachi Bhatt ◽  
Paul Trainor
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Cell Development ◽  
Model System ◽  
Mutant Mice ◽  
Crest Cell

scholarly journals Ca2+ transients in melanocyte dendrites and dendritic spine-like structures evoked by cell-to-cell signaling

2019 ◽  
Vol 219 (1) ◽  
Author(s):  
Rachel L. Belote ◽  
Sanford M. Simon
Keyword(s):  
Cell Signaling ◽  
Neural Crest ◽  
Human Skin ◽  
Dendritic Spine ◽  
Culture System ◽  
Model System ◽  
Process Information ◽  
New Model ◽  
Secreted Factors ◽  
Dendritic Structures

Melanocytes are the neural crest–derived pigment-producing cells of the skin that possess dendrites. Yet little is known about how melanocyte dendrites receive and process information from neighboring cells. Here, using a co-culture system to interrogate the interaction between melanocyte dendrites and keratinocytes, we show that signals from neighboring keratinocytes trigger local compartmentalized Ca2+ transients within the melanocyte dendrites. The localized dendritic Ca2+ transients could be triggered by two keratinocyte-secreted factors, endothelin and acetylcholine, which acted via specific melanocyte receptors. Furthermore, compartmentalized Ca2+ transients were also generated on discrete dendritic spine-like structures on the melanocytes. These spines were also present in intact human skin. Our findings provide insights into how melanocyte dendrites communicate with neighboring cells and offer a new model system for studying compartmentalized signaling in dendritic structures.

scholarly journals The State of the Art of the Zebrafish Model for Toxicology and Toxicologic Pathology Research—Advantages and Current Limitations

2003 ◽  
Vol 31 (1_suppl) ◽  
pp. 62-87 ◽  
Author(s):  
Jan M. Spitsbergen ◽  
Michael L. Kent
Keyword(s):  
Molecular Genetic ◽  
Model System ◽  
Developmental Genetics ◽  
Zebrafish Model ◽  
Vertebrate Model ◽  
Pathologic Lesions ◽  
Minimal Data ◽  
Advanced Knowledge ◽  
The Rich ◽  
Mutant Lines

The zebrafish (Danio rerio ) is now the pre-eminent vertebrate model system for clarification of the roles of specific genes and signaling pathways in development. The zebrafish genome will be completely sequenced within the next 1—2 years. Together with the substantial historical database regarding basic developmental biology, toxicology, and gene transfer, the rich foundation of molecular genetic and genomic data makes zebrafish a powerful model system for clarifying mechanisms in toxicity. In contrast to the highly advanced knowledge base on molecular developmental genetics in zebrafish, our database regarding infectious and noninfectious diseases and pathologic lesions in zebrafish lags far behind the information available on most other domestic mammalian and avian species, particularly rodents. Currently, minimal data are available regarding spontaneous neoplasm rates or spontaneous aging lesions in any of the commonly used wild-type or mutant lines of zebrafish. Therefore, to fully utilize the potential of zebrafish as an animal model for understanding human development, disease, and toxicology we must greatly advance our knowledge on zebrafish diseases and pathology.

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