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.

Cyclical fate restriction: a new view of neural crest cell fate specification

Development ◽  
2021 ◽  
Vol 148 (22) ◽  
Author(s):  
Robert N. Kelsh ◽  
Karen Camargo Sosa ◽  
Saeed Farjami ◽  
Vsevolod Makeev ◽  
Jonathan H. P. Dawes ◽  
...  
Keyword(s):  
Neural Crest ◽  
Cell Fate ◽  
Pigment Cell ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
Dynamic View ◽  
Fate Restriction ◽  
Crest Cell

ABSTRACT Neural crest cells are crucial in development, not least because of their remarkable multipotency. Early findings stimulated two hypotheses for how fate specification and commitment from fully multipotent neural crest cells might occur, progressive fate restriction (PFR) and direct fate restriction, differing in whether partially restricted intermediates were involved. Initially hotly debated, they remain unreconciled, although PFR has become favoured. However, testing of a PFR hypothesis of zebrafish pigment cell development refutes this view. We propose a novel ‘cyclical fate restriction’ hypothesis, based upon a more dynamic view of transcriptional states, reconciling the experimental evidence underpinning the traditional hypotheses.

scholarly journals Regulation of melanocyte development by ligand-dependent BMP signaling underlies oncogenic BMP signaling in melanoma

2019 ◽  
Author(s):  
Alec K. Gramann ◽  
Arvind M. Venkatesan ◽  
Melissa Guerin ◽  
Craig J. Ceol
Keyword(s):  
Neural Crest ◽  
Pigment Cell ◽  
Terminal Differentiation ◽  
Melanoma Cells ◽  
Cell Development ◽  
Bmp Signaling ◽  
Pigment Cells ◽  
Cell Type ◽  
Neural Crest Development ◽  
Direct Regulation

AbstractPreventing terminal differentiation is important in the development and progression of many cancers including melanoma. Recent identification of the BMP ligand GDF6 as a novel melanoma oncogene showed GDF6-activated BMP signaling suppresses differentiation of melanoma cells. Previous studies have identified roles for GDF6 orthologs during early embryonic and neural crest development, but have not identified direct regulation of melanocyte development by GDF6. Here, we investigate the BMP ligand gdf6a, a zebrafish ortholog of human GDF6, during the development of melanocytes from the neural crest. We establish that the loss of gdf6a or inhibition of BMP signaling during neural crest development disrupts normal pigment cell development, leading to an increase in the number of melanocytes and a corresponding decrease in iridophores, another neural crest-derived pigment cell type in zebrafish. This shift occurs as pigment cells arise from the neural crest and depends on mitfa, an ortholog of MITF, a key regulator of melanocyte development that is also targeted by oncogenic BMP signaling. Together, these results indicate that the oncogenic role ligand-dependent BMP signaling plays in suppressing differentiation in melanoma is a reiteration of its physiological roles during melanocyte development.

nacre encodes a zebrafish microphthalmia-related protein that regulates neural-crest-derived pigment cell fate

Development ◽  
1999 ◽  
Vol 126 (17) ◽  
pp. 3757-3767 ◽  
Author(s):  
J.A. Lister ◽  
C.P. Robertson ◽  
T. Lepage ◽  
S.L. Johnson ◽  
D.W. Raible
Keyword(s):  
Transcription Factor ◽  
Retinal Pigment Epithelium ◽  
Neural Crest ◽  
Cell Fate ◽  
Pigment Cell ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Pigment Cells ◽  
Evolutionary Divergence ◽  
Wild Type

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.

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

scholarly journals MON-719 The Cellular and Molecular Landscape of Hypothalamic Patterning and Differentiation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Thomas Kim
Keyword(s):  
Cell Fate ◽  
Regulatory Networks ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Brain Atlas ◽  
Specific Gene ◽  
Cell Fate Specification ◽  
Human Hypothalamus ◽  
Fate Specification ◽  
Time Points

Abstract The hypothalamus is a central regulator of physiological homeostasis. During development, multiple transcription factors coordinate the patterning and specification of hypothalamic nuclei. However, the molecular mechanisms controlling hypothalamic patterning and cell fate specification are poorly understood. To identify genes that control these processes, we have used single-cell RNA sequencing (scRNA-Seq) to profile mouse hypothalamic gene expression across multiple developmental time points. We have further utilised scRNA-Seq to phenotype mutations in genes that play major roles in early hypothalamic patterning. To first understand hypothalamic development, hypothalami were collected at both embryonic (E10-E16, E18) and postnatal (PN4, PN8, PN14, PN45) time points. At early stages, when the bulk of hypothalamic patterning occurs (E11-E13), we observe a clear separation between mitotic progenitors and postmitotic neural precursor cells. We likewise observed clean segregation among cells expressing regional hypothalamic markers identified in previous large-scale analysis of hypothalamic development. This analysis reveals new region-specific markers and identifies candidate genes for selectively regulating patterning and cell fate specification in individual hypothalamic regions. With our rich dataset of developing mouse hypothalamus, we integrated our dataset with the Allen Brain Atlas in situ data, publicly available adult hypothalamic scRNA-Seq dataset to understand hierarchy of hypothalamic cell differentiation, as well as re-defining cell types of the hypothalamus. We next used scRNA-Seq to phenotype multiple mutant lines, including a line that has been extensively characterised as a proof of concept (Ctnnb1 overexpression), and lines that have not been characterised (Nkx2.1, Nkx2.2, Dlx1/2 deletion). We show that this approach can rapidly and comprehensively characterize mutants that have altered hypothalamic patterning, and in doing so, have identified multiple genes that simultaneously repress posterior hypothalamic identity while promoting prethalamic identity. This result supports a modified columnar model of organization for the diencephalon, where prethalamus and hypothalamus are situated in adjacent dorsal and ventral domains of the anterior diencephalon. These data serve as a resource for further studies of hypothalamic development and dysfunction, and able to delineate transcriptional regulatory networks of hypothalamic formation. Lastly, using our mouse hypothalamus as a guideline, we are comparing dataset of developing chicken, zebrafish and human hypothalamus, to identify evolutionarily conserved and divergent region-specific gene regulatory networks. We aim to use this knowledge and information of key molecular pathways of human hypothalamic development and produce human hypothalamus organoids.

scholarly journals Duplication of spiralian-specific TALE genes and evolution of the blastomere specification mechanism in the bivalve lineage

EvoDevo ◽  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Supanat Phuangphong ◽  
Jumpei Tsunoda ◽  
Hiroshi Wada ◽  
Yoshiaki Morino
Keyword(s):  
Cell Fate ◽  
Early Development ◽  
Expression Patterns ◽  
Cell Fate Specification ◽  
Fate Map ◽  
Cell Fates ◽  
Cell Specification ◽  
Cytoplasmic Content ◽  
Gene Regulatory ◽  
Unique Cell

Abstract Background Despite the conserved pattern of the cell-fate map among spiralians, bivalves display several modified characteristics during their early development, including early specification of the D blastomere by the cytoplasmic content, as well as the distinctive fate of the 2d blastomere. However, it is unclear what changes in gene regulatory mechanisms led to such changes in cell specification patterns. Spiralian-TALE (SPILE) genes are a group of spiralian-specific transcription factors that play a role in specifying blastomere cell fates during early development in limpets. We hypothesised that the expansion of SPILE gene repertoires influenced the evolution of the specification pattern of blastomere cell fates. Results We performed a transcriptome analysis of early development in the purplish bifurcate mussel and identified 13 SPILE genes. Phylogenetic analysis of the SPILE gene in molluscs suggested that duplications of SPILE genes occurred in the bivalve lineage. We examined the expression patterns of the SPILE gene in mussels and found that some SPILE genes were expressed in quartet-specific patterns, as observed in limpets. Furthermore, we found that several SPILE genes that had undergone gene duplication were specifically expressed in the D quadrant, C and D quadrants or the 2d blastomere. These expression patterns were distinct from the expression patterns of SPILE in their limpet counterparts. Conclusions These results suggest that, in addition to their ancestral role in quartet specification, certain SPILE genes in mussels contribute to the specification of the C and D quadrants. We suggest that the expansion of SPILE genes in the bivalve lineage contributed to the evolution of a unique cell fate specification pattern in bivalves.

Environmental signals and cell fate specification in premigratory neural crest

BioEssays ◽  
2000 ◽  
Vol 22 (8) ◽  
pp. 708-716 ◽  
Author(s):  
Richard I. Dorsky ◽  
Randall T. Moon ◽  
David W. Raible
Keyword(s):  
Neural Crest ◽  
Cell Fate ◽  
Cell Fate Specification ◽  
Environmental Signals ◽  
Fate Specification
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