Abstract
BackgroundAn intricate gene regulatory network drives neural crest migration and differentiation. How epigenetic regulators contribute to this process is just starting to be understood.ResultsWe found that mutation of med14 or brg1 in zebrafish embryos resulted in a cluster of neural crest cell-related defects. In med14 or brg1 mutants, neural crest cells that form the jaw skeleton were specified normally and migrated to target sites. However, defects in their subsequent terminal differentiation were evident. Transplantation experiments demonstrated that med14 and brg1 are required directly in neural crest cells. Analysis of med14; brg1 double mutant embryos suggested the existence of a strong genetic interaction between members of the Mediator and BAF complexes.ConclusionsThese results suggest a critical role for Mediator and BAF complex function in neural crest development, and may also clarify the nature of defects in some craniofacial abnormalities.
Highlights
An intricate gene regulatory network drives neural crest migration and differentiation
In unrelated studies, we noticed that zebrafish log [10] and young [14] mutants shared a common array of deficiencies in heart, eye, pectoral fin and pigment cell development (Fig. 1a–d and data not shown)
To further investigate the role of med14 and brg1 in development, as well as possible functional interactions between the Mediator and BRG1/BRM-associated factors (BAF) complexes, neural crest cell-derived tissues were analyzed in various mutant backgrounds
Summary
An intricate gene regulatory network drives neural crest migration and differentiation. The specification, migration and differentiation of neural crest cells are tightly coordinated during development, with defects in these processes leading to a number of congenital diseases [2]. There is good evidence that during vertebrate embryogenesis a highly conserved neural crest gene regulatory network (GRN) orchestrates transcriptional events that are critical for various steps of neural crest development [3]. In addition to transcriptional regulation, mounting evidence supports a critical role for epigenetic regulation in neural crest development, most notably by controlling the timing of gene expression during this process [4]. Besides RNA polymerase II, Mediator interacts with and coordinates the action of numerous additional transcriptional regulators, including those acting at the level of chromatin remodeling [7, 8]. We have recently shown that Med plays an essential role in vertebrate embryogenesis and stem cell maintenance [10]
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