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Critical role of Brg1 member of the SWI/SNF chromatin remodeling complex during neurogenesis and neural crest induction in zebrafish
Author(s) -
Eroglu Binnur,
Wang Guanghu,
Tu Naxin,
Sun Xutong,
Mivechi Nahid F.
Publication year - 2006
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20911
Subject(s) - neural crest , neurogenesis , biology , zebrafish , morpholino , swi/snf , microbiology and biotechnology , forebrain , neural development , chromatin remodeling , transcription factor , wnt signaling pathway , genetics , neuroscience , signal transduction , embryo , gene , central nervous system
Brg1 is a member of the SWI/SNF chromatin‐remodeling complex, and in some organisms Brg1 has been shown to interact with β‐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. Developmental Dynamics 235:2722–2735, 2006. © 2006 Wiley‐Liss, Inc.

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