Limits...
Zebrafish endzone regulates neural crest-derived chromatophore differentiation and morphology.

Arduini BL, Gallagher GR, Henion PD - PLoS ONE (2008)

Bottom Line: We have found that although wild-type numbers of chromatophore precursors are generated in the first day of development and migrate normally in enz mutants, the numbers of all three chromatophore cell types that ultimately develop are reduced.Further, differentiated melanophores and xanthophores subsequently lose dendricity, and iridiphores are reduced in size.Our results suggest that enz is required relatively late in the development of all three embryonic chromatophore types and is normally necessary for terminal differentiation and the maintenance of cell size and morphology.

View Article: PubMed Central - PubMed

Affiliation: Center for Molecular Neurobiology, Ohio State University, Columbus, Ohio, United States of America.

ABSTRACT
The development of neural crest-derived pigment cells has been studied extensively as a model for cellular differentiation, disease and environmental adaptation. Neural crest-derived chromatophores in the zebrafish (Danio rerio) consist of three types: melanophores, xanthophores and iridiphores. We have identified the zebrafish mutant endzone (enz), that was isolated in a screen for mutants with neural crest development phenotypes, based on an abnormal melanophore pattern. We have found that although wild-type numbers of chromatophore precursors are generated in the first day of development and migrate normally in enz mutants, the numbers of all three chromatophore cell types that ultimately develop are reduced. Further, differentiated melanophores and xanthophores subsequently lose dendricity, and iridiphores are reduced in size. We demonstrate that enz function is required cell autonomously by melanophores and that the enz locus is located on chromosome 7. In addition, zebrafish enz appears to selectively regulate chromatophore development within the neural crest lineage since all other major derivatives develop normally. Our results suggest that enz is required relatively late in the development of all three embryonic chromatophore types and is normally necessary for terminal differentiation and the maintenance of cell size and morphology. Thus, although developmental regulation of different chromatophore sublineages in zebrafish is in part genetically distinct, enz provides an example of a common regulator of neural crest-derived chromatophore differentiation and morphology.

Show MeSH

Related in: MedlinePlus

The numbers and distribution of chromatophore precursors appear normal in enz homozygotes at 24 hpf.Lateral views of 24 hpf wild-type (A, C, E, G) and enz mutant (B, D, F, H) embryos. Early neural crest cells (crestin; A, B), xanthoblasts (xdh; C, D), melanoblasts (dct; E, F) and all chromatophore precursors (ednrb1; G, H) are all qualitatively normal at this stage.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2483736&req=5

pone-0002845-g004: The numbers and distribution of chromatophore precursors appear normal in enz homozygotes at 24 hpf.Lateral views of 24 hpf wild-type (A, C, E, G) and enz mutant (B, D, F, H) embryos. Early neural crest cells (crestin; A, B), xanthoblasts (xdh; C, D), melanoblasts (dct; E, F) and all chromatophore precursors (ednrb1; G, H) are all qualitatively normal at this stage.

Mentions: Because of the visible defects in neural crest-derived chromatophore development in enz mutant embryos, we investigated whether the development of other cell types derived from the neural crest were affected by the enz mutation. Molecular markers indicated that neural crest-derived peripheral neuron and cranial glial populations develop normally in enz homozygotes (Table 2). For example, cervical sympathetic neurons, enteric neurons, and neurons of the dorsal root ganglia are all present in qualitatively normal numbers and positions in enz mutant embryos (Figure 3 and data not shown). Craniofacial cartilage, stained with alcian blue, was also found to be normal in terms of individual elements and their shapes (Figure 3A, B). In addition, the pan-neural crest marker crestin was used to analyze neural crest populations at different embryonic stages. In wild-type embryos, crestin is first expressed in neural crest cells at the boundary of neural and non-neural ectoderm during gastrulation. Expression continues in premigratory and migratory neural crest cells, and persists until slightly after overt differentiation of neural crest derivatives, such that by 24 hpf, crestin-expressing cells are found throughout the embryo [58]. crestin expression is normal in enz embryos at all stages, indicating that neural crest induction and migration are unaffected by the enz mutation and that neither the proliferation or survival of early neural crest cells are overtly compromised by the enz mutation (Figure 4A, B and data not shown). Further, we examined the expression of genes that, within the neural crest, are expressed by precursors for melanophores, [23], xanthophores [28] and all three chromatophore cell types [37] at 24 hpf. Expression of each gene is qualitatively normal at this stage, suggesting that effects of the enz mutation on crest-derived chromatophores occur relatively late in the development of these cell populations (Figure 4C–H). These data indicate that within the embryonic neural crest lineage, enz is required specifically for chromatophore development and only after neural crest dispersal and initial differentiation have largely occurred.


Zebrafish endzone regulates neural crest-derived chromatophore differentiation and morphology.

Arduini BL, Gallagher GR, Henion PD - PLoS ONE (2008)

The numbers and distribution of chromatophore precursors appear normal in enz homozygotes at 24 hpf.Lateral views of 24 hpf wild-type (A, C, E, G) and enz mutant (B, D, F, H) embryos. Early neural crest cells (crestin; A, B), xanthoblasts (xdh; C, D), melanoblasts (dct; E, F) and all chromatophore precursors (ednrb1; G, H) are all qualitatively normal at this stage.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2483736&req=5

pone-0002845-g004: The numbers and distribution of chromatophore precursors appear normal in enz homozygotes at 24 hpf.Lateral views of 24 hpf wild-type (A, C, E, G) and enz mutant (B, D, F, H) embryos. Early neural crest cells (crestin; A, B), xanthoblasts (xdh; C, D), melanoblasts (dct; E, F) and all chromatophore precursors (ednrb1; G, H) are all qualitatively normal at this stage.
Mentions: Because of the visible defects in neural crest-derived chromatophore development in enz mutant embryos, we investigated whether the development of other cell types derived from the neural crest were affected by the enz mutation. Molecular markers indicated that neural crest-derived peripheral neuron and cranial glial populations develop normally in enz homozygotes (Table 2). For example, cervical sympathetic neurons, enteric neurons, and neurons of the dorsal root ganglia are all present in qualitatively normal numbers and positions in enz mutant embryos (Figure 3 and data not shown). Craniofacial cartilage, stained with alcian blue, was also found to be normal in terms of individual elements and their shapes (Figure 3A, B). In addition, the pan-neural crest marker crestin was used to analyze neural crest populations at different embryonic stages. In wild-type embryos, crestin is first expressed in neural crest cells at the boundary of neural and non-neural ectoderm during gastrulation. Expression continues in premigratory and migratory neural crest cells, and persists until slightly after overt differentiation of neural crest derivatives, such that by 24 hpf, crestin-expressing cells are found throughout the embryo [58]. crestin expression is normal in enz embryos at all stages, indicating that neural crest induction and migration are unaffected by the enz mutation and that neither the proliferation or survival of early neural crest cells are overtly compromised by the enz mutation (Figure 4A, B and data not shown). Further, we examined the expression of genes that, within the neural crest, are expressed by precursors for melanophores, [23], xanthophores [28] and all three chromatophore cell types [37] at 24 hpf. Expression of each gene is qualitatively normal at this stage, suggesting that effects of the enz mutation on crest-derived chromatophores occur relatively late in the development of these cell populations (Figure 4C–H). These data indicate that within the embryonic neural crest lineage, enz is required specifically for chromatophore development and only after neural crest dispersal and initial differentiation have largely occurred.

Bottom Line: We have found that although wild-type numbers of chromatophore precursors are generated in the first day of development and migrate normally in enz mutants, the numbers of all three chromatophore cell types that ultimately develop are reduced.Further, differentiated melanophores and xanthophores subsequently lose dendricity, and iridiphores are reduced in size.Our results suggest that enz is required relatively late in the development of all three embryonic chromatophore types and is normally necessary for terminal differentiation and the maintenance of cell size and morphology.

View Article: PubMed Central - PubMed

Affiliation: Center for Molecular Neurobiology, Ohio State University, Columbus, Ohio, United States of America.

ABSTRACT
The development of neural crest-derived pigment cells has been studied extensively as a model for cellular differentiation, disease and environmental adaptation. Neural crest-derived chromatophores in the zebrafish (Danio rerio) consist of three types: melanophores, xanthophores and iridiphores. We have identified the zebrafish mutant endzone (enz), that was isolated in a screen for mutants with neural crest development phenotypes, based on an abnormal melanophore pattern. We have found that although wild-type numbers of chromatophore precursors are generated in the first day of development and migrate normally in enz mutants, the numbers of all three chromatophore cell types that ultimately develop are reduced. Further, differentiated melanophores and xanthophores subsequently lose dendricity, and iridiphores are reduced in size. We demonstrate that enz function is required cell autonomously by melanophores and that the enz locus is located on chromosome 7. In addition, zebrafish enz appears to selectively regulate chromatophore development within the neural crest lineage since all other major derivatives develop normally. Our results suggest that enz is required relatively late in the development of all three embryonic chromatophore types and is normally necessary for terminal differentiation and the maintenance of cell size and morphology. Thus, although developmental regulation of different chromatophore sublineages in zebrafish is in part genetically distinct, enz provides an example of a common regulator of neural crest-derived chromatophore differentiation and morphology.

Show MeSH
Related in: MedlinePlus