Lou Xin, Burrows Jeffrey T A, Scott Ian C
Model Animal Research Center, Nanjing University, 12 Xuefu Road, Nanjing, 210061, Jiangsu, China.
Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, 686 Bay Street, Toronto, Ontario, M5G 0A4, Canada.
BMC Dev Biol. 2015 Nov 9;15:41. doi: 10.1186/s12861-015-0090-9.
An intricate gene regulatory network drives neural crest migration and differentiation. How epigenetic regulators contribute to this process is just starting to be understood.
We 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.
These 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.
一个复杂的基因调控网络驱动神经嵴的迁移和分化。表观遗传调控因子如何参与这一过程才刚刚开始被理解。
我们发现斑马鱼胚胎中med14或brg1的突变导致了一系列与神经嵴细胞相关的缺陷。在med14或brg1突变体中,形成颌骨骨架的神经嵴细胞正常特化并迁移到目标位点。然而,它们随后的终末分化缺陷明显。移植实验表明med14和brg1在神经嵴细胞中是直接必需的。对med14;brg1双突变胚胎的分析表明,中介体复合物和BAF复合物成员之间存在强烈的遗传相互作用。
这些结果表明中介体和BAF复合物功能在神经嵴发育中起关键作用,也可能阐明一些颅面异常缺陷的本质。