Xanthophores in chromatophore groups of the premigratory neural crest initiate the pigment pattern of the axolotl larva

1984 ◽  
Vol 193 (6) ◽  
pp. 357-369 ◽  
Author(s):  
Hans Henning Epperlein ◽  
Jan L�fberg
Keyword(s):  
Neural Crest ◽  
Pigment Pattern

scholarly journals Embryonic requirements for ErbB signaling in neural crest development and adult pigment pattern formation

Development ◽  
2008 ◽  
Vol 135 (15) ◽  
pp. 2603-2614 ◽  
Author(s):  
E. H. Budi ◽  
L. B. Patterson ◽  
D. M. Parichy
Keyword(s):  
Pattern Formation ◽  
Neural Crest ◽  
Pigment Pattern ◽  
Neural Crest Development ◽  
Erbb Signaling

Mechanisms of pigment pattern formation in the quail embryo

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 81-89 ◽  
Author(s):  
M.K. Richardson ◽  
A. Hornbruch ◽  
L. Wolpert
Keyword(s):  
Pattern Formation ◽  
Neural Crest ◽  
Larval Fish ◽  
Dorsal Surface ◽  
Neural Crest Cells ◽  
Mirror Image ◽  
Differential Migration ◽  
Pigment Pattern ◽  
Pigment Patterns ◽  
Local Cues

One hypothesis to account for pigment patterning in birds is that neural crest cells migrate into all feather papillae. Local cues then act upon the differentiation of crest cells into melanocytes. This hypothesis is derived from a study of the quail-chick chimaera (Richardson et al., Development 107, 805–818, 1989). Another idea, derived from work on larval fish and amphibia, is that pigment patterns arise from the differential migration of crest cells. We want to know which of these mechanisms can best account for pigment pattern formation in the embryonic plumage of the quail wing. Most of the feather papillae on the dorsal surface of the wing are pigmented, while many on the ventral surface are white. When ectoderm from unpigmented feather papillae is grown in culture, it gives rise to melanocytes. This indicates that neural crest cells are present in white feathers but that they fail to differentiate. If the wing tip is inverted experimentally then the pigment pattern is inverted also. This is difficult to explain in terms of a model based on migratory pathways, unless one assumes that the pathways became re-routed. When an extra polarizing region is grafted to the anterior margin of the wing bud, a duplication develops in: (1) the pattern of skeletal elements; (2) the pattern of feather papillae; (3) the feather pigment pattern. The pigment pattern was not a precise mirror image although some groups of papillae showed a high degree of symmetry in their pigmentation. Both the tip inversions and the duplications produce discontinuities in the feather and pigment patterns. No evidence of intercalation was found in these cases. We conclude that pigment patterning in birds is determined by local cues acting on melanocyte differentiation, rather than by the differential migration of crest cells. Positional values along the anteroposterior axis of the pigment pattern are determined by a gradient of positional information. Thus the pigment patterns, feather patterns and cartilage patterns of the wing may all be specified by a similar mechanism.

Melanoblast-tissue interactions and the development of pigment pattern in Xenopus larvae

Development ◽  
1976 ◽  
Vol 35 (3) ◽  
pp. 463-484
Author(s):  
Gillian J. MacMillan
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Population Pressure ◽  
Primary Host ◽  
Pigment Pattern ◽  
Embryonic Tissues ◽  
Tissue Interactions ◽  
Species Specific ◽  
Almost All ◽  
Neural Crest Migration

The melanophores of larval Xenopus laevis are disparately distributed on the hypomere in that the upper region (UHT) is densely pigmented, the median region (MHT) is moderately pigmented, and the lower region (LHT) is unpigmented. The roles of the melanoblasts and their tissue environment in determining the melanophore pattern was investigated by heterotopic transplantation of hypomeric tissues, culture of neural crest explants in vesicles derived from hypomeric tissues and radioactive marking of neural crest cells. Somite-situated grafts of UHT, MHT and LHT were found to possess melanophore densities similar to those exhibited by such hypomeric tissues when in their normal situation. The number and distribution of trunk melanophores in ‘crestless’ second host larvae bearing grafts of UHT, MHT and LHT transferred from the somites of primary host embryos indicated that (a) many melanoblasts entered all transplants during neural crest migration in the primary host: subsequently, a small number of melanoblasts were lost from transplants of UHT, a greater number from transplants of MHT and almost all from transplants of LHT; (b) almost all melanoblasts migrated out from transplants of MHT and LHT and entered the tissues of the ‘crestless’ host, whereas a considerable number of melanoblasts remained in the transplant when it was formed from UHT. Grafts of UHT placed mid-ventrally in the hypomere failed to exhibit melanophores. Vesicles of (a) UHT + MHT and (b) LHT containing neural crest tissue possessed similar numbers of melanophores. Vesicles of LHT differed from those of UHT + MHT in that melanophores were densely aggregated in the implanted neural tissues. Following radioactive marking of neural crest cells labelled nuclei were found on the dorsal ridges of the somites, the surfaces of the neural tube and notochord and in the mesoderm of the upper hypomere and the fin, but were absent from the lateral surfaces of the somites. These results showed that the melanophore pattern in larval Xenopus depended upon melanoblast-tissue interactions, which influenced the migration, rather than the differentiation, proliferation or destruction, of melanoblasts and suggested that tissue selection by migrating melanoblasts enabled these cells to distribute themselves in embryonic tissues in accordance with a hierarchy of melanoblast-tissue affinities. Melanoblast-tissue affinities appeared to be related to the adhesiveness of mesodermal cells: melanoblast extensibility appeared to facilitate exploration of the surrounding tissues. The formation of pigment pattern in larval Xenopus appeared to depend upon the interaction between the melanoblast population pressure and melanoblast-tissue affinities. The present results and those of other workers on amphibian pigmentation were used toconstruct a model capable of accounting for species-specific differences in larval amphibian pigment patterns, in terms of interactions between species-specific differences in melanoblast-tissue affinities and melanoblast population pressure.

scholarly journals Mutational Analysis of Endothelin Receptor b1 (rose) during Neural Crest and Pigment Pattern Development in the Zebrafish Danio rerio

2000 ◽  
Vol 227 (2) ◽  
pp. 294-306 ◽  
Author(s):  
David M. Parichy ◽  
Eve M. Mellgren ◽  
John F. Rawls ◽  
Susana S. Lopes ◽  
Robert N. Kelsh ◽  
...  
Keyword(s):  
Neural Crest ◽  
Danio Rerio ◽  
Mutational Analysis ◽  
Endothelin Receptor ◽  
Pigment Pattern ◽  
Pattern Development

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.

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.

Zebrafish pigmentation mutations and the processes of neural crest development

Development ◽  
1996 ◽  
Vol 123 (1) ◽  
pp. 369-389 ◽  
Author(s):  
R.N. Kelsh ◽  
M. Brand ◽  
Y.J. Jiang ◽  
C.P. Heisenberg ◽  
S. Lin ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Fate ◽  
Large Scale ◽  
Pigment Cell ◽  
Cell Fate Specification ◽  
Cell Specification ◽  
Pigment Pattern ◽  
Mutagenesis Screen ◽  
Neural Crest Development

Neural crest development involves cell-fate specification, proliferation, patterned cell migration, survival and differentiation. Zebrafish neural crest derivatives include three distinct chromatophores, which are well-suited to genetic analysis of their development. As part of a large-scale mutagenesis screen for embryonic/early larval mutations, we have isolated 285 mutations affecting all aspects of zebrafish larval pigmentation. By complementation analysis, we define 94 genes. We show here that comparison of their phenotypes permits classification of these mutations according to the types of defects they cause, and these suggest which process of neural crest development is probably affected. Mutations in eight genes affect the number of chromatophores: these include strong candidates for genes necessary for the processes of pigment cell specification and proliferation. Mutations in five genes remove part of the wild-type pigment pattern, and suggest a role in larval pigment pattern formation. Mutations in five genes show ectopic chromatophores in distinct sites, and may have implications for chromatophore patterning and proliferation. 76 genes affect pigment or morphology of one or more chromatophore types: these mutations include strong candidates for genes important in various aspects of chromatophore differentiation and survival. In combination with the embryological advantages of zebrafish, these mutations should permit cellular and molecular dissection of many aspects of neural crest development.

scholarly journals Pax7 is required for establishment of the xanthophore lineage in zebrafish embryos

2016 ◽  
Vol 27 (11) ◽  
pp. 1853-1862 ◽  
Author(s):  
Hanna Nord ◽  
Nils Dennhag ◽  
Joscha Muck ◽  
Jonas von Hofsten
Keyword(s):  
Neural Crest ◽  
Double Mutant ◽  
Zebrafish Embryo ◽  
Animal Species ◽  
Precursor Cells ◽  
Zebrafish Embryos ◽  
Adult Zebrafish ◽  
Pigment Pattern ◽  
Severe Reduction ◽  
Different Types

The pigment pattern of many animal species is a result of the arrangement of different types of pigment-producing chromatophores. The zebrafish has three different types of chromatophores: black melanophores, yellow xanthophores, and shimmering iridophores arranged in a characteristic pattern of golden and blue horizontal stripes. In the zebrafish embryo, chromatophores derive from the neural crest cells. Using pax7a and pax7b zebrafish mutants, we identified a previously unknown requirement for Pax7 in xanthophore lineage formation. The absence of Pax7 results in a severe reduction of xanthophore precursor cells and a complete depletion of differentiated xanthophores in embryos as well as in adult zebrafish. In contrast, the melanophore lineage is increased in pax7a/pax7b double-mutant embryos and larvae, whereas juvenile and adult pax7a/pax7b double-mutant zebrafish display a severe decrease in melanophores and a pigment pattern disorganization indicative of a xanthophore- deficient phenotype. In summary, we propose a novel role for Pax7 in the early specification of chromatophore precursor cells.

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.

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