Tfap2 transcription factors in zebrafish neural crest development and ectodermal evolution

2007 ◽  
Vol 308B (5) ◽  
pp. 679-691 ◽  
Author(s):  
Trevor L. Hoffman ◽  
Anna L. Javier ◽  
Shelley A. Campeau ◽  
Robert D. Knight ◽  
Thomas F. Schilling
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Neural Crest Development

The winged-helix transcription factor FoxD3 is important for establishing the neural crest lineage and repressing melanogenesis in avian embryos

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1467-1479 ◽  
Author(s):  
R. Kos ◽  
M.V. Reedy ◽  
R.L. Johnson ◽  
C.A. Erickson
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Antisense Oligonucleotides ◽  
Neural Crest Cells ◽  
Winged Helix ◽  
Dorsal Neural Tube ◽  
Neural Crest Development ◽  
Mesenchymal Transformation ◽  
Winged Helix Transcription Factor

The winged-helix or forkhead class of transcription factors has been shown to play important roles in cell specification and lineage segregation. We have cloned the chicken homolog of FoxD3, a member of the winged-helix class of transcription factors, and analyzed its expression. Based on its expression in the dorsal neural tube and in all neural crest lineages except the late-emigrating melanoblasts, we predicted that FoxD3 might be important in the segregation of the neural crest lineage from the neural epithelium, and for repressing melanogenesis in early-migrating neural crest cells. Misexpression of FoxD3 by electroporation in the lateral neural epithelium early in neural crest development produced an expansion of HNK1 immunoreactivity throughout the neural epithelium, although these cells did not undergo an epithelial/mesenchymal transformation. To test whether FoxD3 represses melanogenesis in early migrating neural crest cells, we knocked down expression in cultured neural crest with antisense oligonucleotides and in vivo by treatment with morpholino antisense oligonucleotides. Both experimental approaches resulted in an expansion of the melanoblast lineage, probably at the expense of neuronal and glial lineages. Conversely, persistent expression of FoxD3 in late-migrating neural crest cells using RCAS viruses resulted in the failure of melanoblasts to develop. We suggest that FoxD3 plays two important roles in neural crest development. First, it is involved in the segregation of the neural crest lineage from the neuroepithelium. Second, it represses melanogenesis, thereby allowing other neural crest derivatives to differentiate during the early stages of neural crest patterning.

scholarly journals Discovery of transcription factors and other candidate regulators of neural crest development

2008 ◽  
Vol 237 (4) ◽  
pp. 1021-1033 ◽  
Author(s):  
Meghan S. Adams ◽  
Laura S. Gammill ◽  
Marianne Bronner-Fraser
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Neural Crest Development

scholarly journals Regulation of sarcomagenesis by the empty spiracles homeobox genes EMX1 and EMX2

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Manuel Pedro Jimenez-García ◽  
Antonio Lucena-Cacace ◽  
Daniel Otero-Albiol ◽  
Amancio Carnero
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Transcription Factors ◽  
Neural Crest ◽  
Tumor Suppressors ◽  
Homeobox Genes ◽  
Neuronal Cell ◽  
Cell Gene Expression

AbstractThe EMX (Empty Spiracles Homeobox) genes EMX1 and EMX2 are two homeodomain gene members of the EMX family of transcription factors involved in the regulation of various biological processes, such as cell proliferation, migration, and differentiation, during brain development and neural crest migration. They play a role in the specification of positional identity, the proliferation of neural stem cells, and the differentiation of certain neuronal cell phenotypes. In general, they act as transcription factors in early embryogenesis and neuroembryogenesis from metazoans to higher vertebrates. The EMX1 and EMX2’s potential as tumor suppressor genes has been suggested in some cancers. Our work showed that EMX1/EMX2 act as tumor suppressors in sarcomas by repressing the activity of stem cell regulatory genes (OCT4, SOX2, KLF4, MYC, NANOG, NES, and PROM1). EMX protein downregulation, therefore, induced the malignance and stemness of cells both in vitro and in vivo. In murine knockout (KO) models lacking Emx genes, 3MC-induced sarcomas were more aggressive and infiltrative, had a greater capacity for tumor self-renewal, and had higher stem cell gene expression and nestin expression than those in wild-type models. These results showing that EMX genes acted as stemness regulators were reproduced in different subtypes of sarcoma. Therefore, it is possible that the EMX genes could have a generalized behavior regulating proliferation of neural crest-derived progenitors. Together, these results indicate that the EMX1 and EMX2 genes negatively regulate these tumor-altering populations or cancer stem cells, acting as tumor suppressors in sarcoma.

scholarly journals The methyltransferase NSD3 regulates neural crest development

2011 ◽  
Vol 356 (1) ◽  
pp. 196
Author(s):  
Bridget Jacques-Fricke ◽  
Laura S. Gammill
Keyword(s):  
Neural Crest ◽  
Neural Crest Development
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