TL;DR: It is demonstrated that melanophore development in fish and mammals shares a dependence on the nacre/Mitf transcription factor, but that proper development of the retinal pigment epithelium in the fish is not nacre-dependent, suggesting an evolutionary divergence in the function of this gene.
Abstract: We report the isolation and identification of a new mutation affecting pigment cell fate in the zebrafish neural crest. Homozygous nacre (nac(w2)) mutants lack melanophores throughout development but have increased numbers of iridophores. The non-crest-derived retinal pigment epithelium is normal, suggesting that the mutation does not affect pigment synthesis per se. Expression of early melanoblast markers is absent in nacre mutants and transplant experiments suggested a cell-autonomous function in melanophores. We show that nac(w2) is a mutation in a zebrafish gene encoding a basic helix-loop-helix/leucine zipper transcription factor related to microphthalmia (Mitf), a gene known to be required for development of eye and crest pigment cells in the mouse. Transient expression of the wild-type nacre gene restored melanophore development in nacre(-/-) embryos. Furthermore, misexpression of nacre induced the formation of ectopic melanized cells and caused defects in eye development in wild-type and mutant embryos. These results demonstrate that melanophore development in fish and mammals shares a dependence on the nacre/Mitf transcription factor, but that proper development of the retinal pigment epithelium in the fish is not nacre-dependent, suggesting an evolutionary divergence in the function of this gene.
TL;DR: It is demonstrated that colourless mutant neural crest cells form ectomesenchymal fates, which suggests a novel mechanism for the aetiology of Waardenburg-Shah syndrome in which affected neural crest derivatives fail to be generated from the neural crest.
Abstract: Waardenburg-Shah syndrome combines the reduced enteric nervous system characteristic of Hirschsprung's disease with reduced pigment cell number, although the cell biological basis of the disease is unclear. We have analysed a zebrafish Waardenburg-Shah syndrome model. We show that the colourless gene encodes a sox10 homologue, identify sox10 lesions in mutant alleles and rescue the mutant phenotype by ectopic sox10 expression. Using iontophoretic labelling of neural crest cells, we demonstrate that colourless mutant neural crest cells form ectomesenchymal fates. By contrast, neural crest cells which in wild types form non-ectomesenchymal fates generally fail to migrate and do not overtly differentiate. These cells die by apoptosis between 35 and 45 hours post fertilisation. We provide evidence that melanophore defects in colourless mutants can be largely explained by disruption of nacre/mitf expression. We propose that all defects of affected crest derivatives are consistent with a primary role for colourless/sox10 in specification of non-ectomesenchymal crest derivatives. This suggests a novel mechanism for the aetiology of Waardenburg-Shah syndrome in which affected neural crest derivatives fail to be generated from the neural crest.
TL;DR: Pale coloration ranging from tan to green is provided by the overlying xanthophores and iridophores, and the nature of the intimate contact between the chromatophore types is discussed.
Abstract: Rapid color changes of amphibians are mediated by three types of dermal chromatophores, xanthophores, iridophores, and melanophores, which comprise a morphologically and physiologically distinct structure, the dermal chromatophore unit. Xanthophores, the outermost element, are located immediately below the basal lamella. Iridophores, containing light-reflecting organelles, are found just beneath the xanthophores. Under each iridophore is found a melanophore from which processes extend upward around the iridophore. Finger-like structures project from these processes and occupy fixed spaces between the xanthophores and iridophores. When a frog darkens, melanosomes move upward from the body of the melanophore to fill the fingers which then obscure the overlying iridophore. Rapid blanching is accomplished by the evacuation of melanosomes from these fingers. Pale coloration ranging from tan to green is provided by the overlying xanthophores and iridophores. Details of chromatophore structure are presented, and the nature of the intimate contact between the chromatophore types is discussed.
TL;DR: It is reasoned from observations made on the kinetics of pigment migration within the processes of these melanophores that the microtubules function as cytoskeletal elements which help maintain the extended form of the melanophore arms and at the same time define the channels in which the pigment moves.
Abstract: The dermal melanophores ofFundulus heteroclitus L have been investigated by light and electron microscopy with the purpose of revealing the mechanisms controlling pigment migration As predicted by earlier studies, the nerve endings of a double innervation were found adjacent to and in synaptic relation to the melanophore surface Not expected were the large number of small pits or invaginations present in the cell surface These appear identical to the so-called micropinocytotic vesicles found generally in cells of the vascular endothalium and smooth muscle In chromatophores they are more reasonably interpreted as receptor sites for neurohormones than as uptake and transport mechanisms Observations made on the kinetics of pigment migration within the processes of these melanophores indicate that the granules move along relatively fixed channels arranged parallel to the long axes of the processes Examined at fine structure levels, the zones of cytoplasm around these channels are found to be populated by microtubules about 225 A in diameter aligned parallel to the direction of pigment movement These long slender elements are present in the processes regardless of whether the melanin is concentrated in the cell center or dispersed It is reasoned from these and other observations that the microtubules function as cytoskeletal elements which help maintain the extended form of the melanophore arms and at the same time define the channels in which the pigment moves The possible role of the tubule in generating the motive force for pigment migration is discussed
TL;DR: The model systems discussed here - chick, mouse, and zebrafish - each provide unique insights into the major morphogenetic events driving pigment pattern formation, and the current understanding of the mechanisms regulating melanoblast number and organization in the epidermis is summarized.