Intercellular Relations in the Development of Amphibian Pigmentation

Development ◽  
1953 ◽  
Vol 1 (3) ◽  
pp. 263-268
Author(s):  
Victor C. Twitty
Keyword(s):  
Neural Crest ◽  
Pigment Cells ◽  
Pigment Pattern ◽  
Present Discussion ◽  
Amoeboid Cells

The role of intercellular influences in the control of differentiation finds many illustrations in the development of amphibian pigmentation. From the time the chromatophores leave the neural crest as colourless, amoeboid cells, until they come to rest as differentiated elements of the distinctive pigment pattern, their developmental behaviour is conditioned throughout by effects exerted mutually by the chromatophores themselves or imposed upon them by the cells of neighbouring tissues. For the purposes of the present discussion, I shall limit myself to examples of intercellular relations affecting (1) the migration of chromatoblasts and (2) their synthesis of pigment. Various suggestions have been made concerning the nature of the factors responsible for the dispersion of pro-pigment cells from the mid-dorsal line to their resting-places throughout the skin. One is that the cells are actually drawn ventrally in response to a true chemotactic attraction exerted by the skin beneath which they spread.

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

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.

scholarly journals Endothelin receptor Aa regulates proliferation and differentiation of Erb-dependant pigment progenitors in zebrafish

2018 ◽  
Author(s):  
Karen Camargo-Sosa ◽  
Sarah Colanesi ◽  
Jeanette Müller ◽  
Stefan Schulte-Merker ◽  
Derek Stemple ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Crest ◽  
Blood Vessels ◽  
Communication Process ◽  
Pigment Cells ◽  
Quiescent State ◽  
Dependent Manner ◽  
Endothelin Receptor ◽  
Pigment Pattern ◽  
Pigment Patterns

AbstractSkin pigment patterns are important, being under strong selection for multiple roles including camouflage and UV protection. Pigment cells underlying these patterns form from adult pigment stem cells (APSCs). In zebrafish, APSCs derive from embryonic neural crest cells, but sit dormant until activated to produce pigment cells during metamorphosis. The APSCs are set-aside in an ErbB signaling dependent manner, but the mechanism maintaining quiescence until metamorphosis remains unknown. Mutants for a pigment pattern gene, parade, exhibit ectopic pigment cells localised to the ventral trunk. We show that parade encodes Endothelin receptor Aa, expressed in the blood vessels. Using chemical genetics, coupled with analysis of cell fate studies, we show that the ectopic pigment cells derive from APSCs. We propose that a novel population of APSCs exists in association with medial blood vessels, and that their quiescence is dependent upon Endothelin-dependent factors expressed by the blood vessels.Lay AbstractPigment patterns are crucial for the many aspects of animal biology, for example, providing camouflage, enabling mate selection and protecting against UV irradiation. These patterns are generated by one or more pigment cell-types, localised in the skin, but derived from specialised stem cells (adult pigment stem cells, APSCs). In mammals, such as humans, but also in birds and fish, these APSCs derive from a transient population of multipotent progenitor cells, the neural crest. Formation of the adult pigment pattern is perhaps best studied in the zebrafish, where the adult pigment pattern is formed during a metamorphosis beginning around 21 days of development. The APSCs are set-aside in the embryo around 1 day of development, but then remain inactive until that metamorphosis, when they become activated to produce the adult pigment cells. We know something of how the cells are set-aside, but what signals maintain them in an inactive state is a mystery. Here we study a zebrafish mutant, called parade, which shows ectopic pigment cells in the embryo. We clone the parade gene, identifying it as ednraa encoding a component of a cell-cell communication process, which is expressed in blood vessels. By characterising the changes in the neural crest and in the pigment cells formed, and by combining this with an innovative assay identifying drugs that prevent the ectopic cells from forming, we deduce that the ectopic cells in the larva derive from precocious activation of APSCs to form pigment cells. We propose that a novel population of APSCs are associated with the blood vessels, that these are held in a quiescent state by signals coming from these vessels, and that these signals depend upon ednraa. Together this opens up an exciting opportunity to identify the signals maintaining APSC quiescence in zebrafish.

An orthologue of the kit-related gene fms is required for development of neural crest-derived xanthophores and a subpopulation of adult melanocytes in the zebrafish, Danio rerio

Development ◽  
2000 ◽  
Vol 127 (14) ◽  
pp. 3031-3044 ◽  
Author(s):  
D.M. Parichy ◽  
D.G. Ransom ◽  
B. Paw ◽  
L.I. Zon ◽  
S.L. Johnson
Keyword(s):  
Neural Crest ◽  
Danio Rerio ◽  
Receptor Tyrosine Kinase ◽  
Pigment Cell ◽  
Pigment Cells ◽  
Pigment Pattern ◽  
Cell Behaviors ◽  
Pattern Development ◽  
And Migration ◽  
Pigment Patterns

Developmental mechanisms underlying traits expressed in larval and adult vertebrates remain largely unknown. Pigment patterns of fishes provide an opportunity to identify genes and cell behaviors required for postembryonic morphogenesis and differentiation. In the zebrafish, Danio rerio, pigment patterns reflect the spatial arrangements of three classes of neural crest-derived pigment cells: black melanocytes, yellow xanthophores and silver iridophores. We show that the D. rerio pigment pattern mutant panther ablates xanthophores in embryos and adults and has defects in the development of the adult pattern of melanocyte stripes. We find that panther corresponds to an orthologue of the c-fms gene, which encodes a type III receptor tyrosine kinase and is the closest known homologue of the previously identified pigment pattern gene, kit. In mouse, fms is essential for the development of macrophage and osteoclast lineages and has not been implicated in neural crest or pigment cell development. In contrast, our analyses demonstrate that fms is expressed and required by D. rerio xanthophore precursors and that fms promotes the normal patterning of melanocyte death and migration during adult stripe formation. Finally, we show that fms is required for the appearance of a late developing, kit-independent subpopulation of adult melanocytes. These findings reveal an unexpected role for fms in pigment pattern development and demonstrate that parallel neural crest-derived pigment cell populations depend on the activities of two essentially paralogous genes, kit and fms.

scholarly journals Critical role of Brg1 member of the SWI/SNF chromatin remodeling complex during neurogenesis and neural crest induction in zebrafish

2006 ◽  
Vol 235 (10) ◽  
pp. 2722-2735 ◽  
Author(s):  
Binnur Eroglu ◽  
Guanghu Wang ◽  
Naxin Tu ◽  
Xutong Sun ◽  
Nahid F. Mivechi
Keyword(s):  
Neural Crest ◽  
Chromatin Remodeling ◽  
Critical Role ◽  
Chromatin Remodeling Complex

scholarly journals The Role of Neural Crest during Cardiac Development in a Mouse Model of DiGeorge Syndrome

2002 ◽  
Vol 251 (1) ◽  
pp. 157-166 ◽  
Author(s):  
Lazaros Kochilas ◽  
Sandra Merscher-Gomez ◽  
Min Min Lu ◽  
Vijaya Potluri ◽  
Jun Liao ◽  
...  
Keyword(s):  
Mouse Model ◽  
Neural Crest ◽  
Digeorge Syndrome ◽  
Cardiac Development

Developmental potential of neural crest-derived cells migrating from segments of developing quail bowel back-grafted into younger chick host embryos

Development ◽  
1990 ◽  
Vol 109 (2) ◽  
pp. 411-423 ◽  
Author(s):  
T.P. Rothman ◽  
N.M. Le Douarin ◽  
J.C. Fontaine-Perus ◽  
M.D. Gershon
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Peripheral Nerves ◽  
Sympathetic Ganglia ◽  
Limb Bud ◽  
Pigment Cells ◽  
Developmental Potential ◽  
Migratory Experience ◽  
Host Embryo

The technique of back-transplantation was used to investigate the developmental potential of neural crest-derived cells that have migrated to and colonized the avian bowel. Segments of quail bowel (removed at E4) were grafted between the somites and neural tube of younger (E2) chick host embryos. Grafts were placed at a truncal level, adjacent to somites 14–24. Initial experiments, done in vitro, confirmed that crest-derived cells are capable of migrating out of segments of foregut explanted at E4. The foregut, which at E4 has been colonized by cells derived from the vagal crest, served as the donor tissue. Comparative observations were made following grafts of control tissues, which included hindgut, lung primordia, mesonephros and limb bud. Additional experiments were done with chimeric bowel in which only the crest-derived cells were of quail origin. Targets in the host embryos colonized by crest-derived cells from the foregut grafts included the neural tube, spinal roots and ganglia, peripheral nerves, sympathetic ganglia and the adrenals, but not the gut. Donor cells in these target organs were immunostained by the monoclonal antibody, NC-1, indicating that they were crest-derived and developing along neural or glial lineages. Some of the crest-derived cells (NC-1-immunoreactive) that left the bowel and reached sympathetic ganglia, but not peripheral nerves or dorsal root ganglia, co-expressed tyrosine hydroxylase immunoreactivity, a neural characteristic never expressed by crest-derived cells in the avian gut. None of the cells leaving enteric back-grafts produced pigment. Cells of mesodermal origin were also found to leave donor explants and aggregate in dermis and feather germs near the grafts. These observations indicate that crest-derived cells, having previously migrated to the bowel, retain the ability to migrate to distant sites in a younger embryo. The routes taken by these cells appear to reflect, not their previous migratory experience, but the level of the host embryo into which the graft is placed. Some of the population of crest-derived cells that leave the back-transplanted gut remain capable of expressing phenotypes that they do not express within the bowel in situ, but which are appropriate for the site in the host embryo to which they migrate.

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