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ZFIN ID: ZDB-PUB-060816-18
Critical role of Brg1 member of the SWI/SNF chromatin remodeling complex during neurogenesis and neural crest induction in zebrafish
Eroglu, B., Wang, G., Tu, N., Sun, X., and Mivechi, N.F.
Date: 2006
Source: Developmental dynamics : an official publication of the American Association of Anatomists 235(10): 2722-2735 (Journal)
Registered Authors:
Keywords: zebrafish, Brg1 mutant (yng), morpholino, neurogenesis, neural crest
MeSH Terms:
  • Adaptor Proteins, Signal Transducing
  • Animals
  • Cell Differentiation/genetics
  • Cell Differentiation/physiology
  • Chromatin/metabolism
  • Chromatin Immunoprecipitation
  • Chromosomal Proteins, Non-Histone/genetics
  • Chromosomal Proteins, Non-Histone/metabolism
  • Chromosomal Proteins, Non-Histone/physiology*
  • DNA Helicases/genetics
  • DNA Helicases/metabolism
  • DNA Helicases/physiology
  • Embryo, Nonmammalian/embryology
  • Embryo, Nonmammalian/metabolism
  • Gene Expression Regulation, Developmental/genetics
  • Immunohistochemistry
  • In Situ Hybridization
  • Mutation/genetics
  • Neural Crest/embryology*
  • Neural Crest/metabolism
  • Organogenesis/genetics
  • Organogenesis/physiology
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Time Factors
  • Transcription Factors/genetics
  • Transcription Factors/metabolism
  • Transcription Factors/physiology*
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Zebrafish Proteins/physiology*
PubMed: 16894598 Full text @ Dev. Dyn.
FIGURES
ABSTRACT
Brg1 is a member of the SWI/SNF chromatin-remodeling complex, and in some organisms Brg1 has been shown to interact with beta-catenin and positively control the TCF/LEF transcription factor that is located downstream of the Wnt signal transduction pathway. During development, TCF/LEF activity is critical during neurogenesis and head induction. In zebrafish, Brg1-deficient embryos exhibit retinal cell differentiation and eye defects; however, the role of Brg1 in neurogenesis and neural crest cell induction remains elusive. We used zebrafish deficient in Brg1 (yng) or Brg1 specific-morpholino oligonucleotide-mediated knockdown to analyze the embryonic requirements of Brg1. Our results indicate that reduction in Brg1 expression leads to the expansion of the forebrain-specific transcription factor, six3, and marked reduction in expression of the mid/hind-brain boundary and hind-brain genes, engrailed2 and krox20, respectively. At 12 hpf, the expression of neural crest specifiers are severely affected in Brg1-morpholino-injected embryos. These results suggest that Brg1 is involved in neural crest induction, which is critical for the development of neurons, glia, pigment cells, and craniofacial structures. Brg1 is a maternal factor, and brg1-deficient embryos bearing the yng mutation derived from heterozygote intercrosses exhibit lesser effects on neural crest-specific gene expression, but show defects in neurogenesis and neural crest cell differentiation. This is exhibited by the aberrant brain patterning, a reduction in the sensory neurons, and craniofacial defects. These results further elucidate the critical role for Brg1 in neurogenesis, neural crest induction, and differentiation.
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