Zebrafish narrowminded disrupts the transcription factor prdm1 and is required for neural crest and sensory neuron specification
Zebrafish narrowminded disrupts the transcription factor prdm1 and is required for neural crest and sensory neuron specification
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DOI：
10.1016/j.ydbio.2004.11.014
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发表时间：
2005-02-15
影响因子：
2.7
通讯作者：
Artinger, KB
中科院分区：
文献类型：
--
作者：
Hernandez-Lagunas, L;Choi, IF;Artinger, KB
神经嵴细胞和Robon-Beard（RB）感觉神经元的特化涉及神经和非神经外胚层之间的一系列复杂的相互作用。指导这一过程的分子机制还不清楚。斑马鱼的narrowminded（nrd）突变是独特的，因为它是两种细胞群体中观察到缺陷的两种突变之一：它导致RB神经元的完全缺失和神经嵴细胞及其衍生物的减少。在这里，我们表明，nrd是一个突变prdm 1，SET/锌指结构域转录因子。一个吗啉代介导的消耗prdm 1 phenocopies的nrd突变，并反过来过表达prdm 1 mRNA拯救nrd RB感觉神经元和神经嵴表型。prdm 1在神经嵴细胞和RB感觉神经元形成的区域内的神经板的边界处表达。通过过表达对prdm 1功能的分析表明，prdm 1的功能是促进神经嵴细胞和RB感觉神经元的细胞命运特化，最有可能作为BMP信号传导途径的下游效应物。(C)2004年爱思唯尔公司All rights reserved.
Specification of both neural crest cells and Robon-Beard (RB) sensory neurons involves a complex series of interactions between the neural and non-neural ectoderm. The molecular mechanisms directing this process are not well understood. The zebrafish narrowminded (nrd) mutation is unique, since it is one of two mutations in which defects are observed in both cell populations: it leads to a complete absence of RB neurons and a reduction in neural crest cells and their derivatives. Here, we show that nrd is a mutation in prdm1, a SET/zinc-finger domain transcription factor. A Morpholino-mediated depletion of prdm1 phenocopies the nrd mutation, and conversely overexpression of prdm1 mRNA rescues the nrd RB sensory neuron and neural crest phenotype. prdm1 is expressed at the border of the neural plate within the domain where neural crest cells and RB sensory neurons form. Analysis of prdm1 function by overexpression indicates that prdm1 functions to promote the cell fate specification of both neural crest cells and RB sensory neurons, most likely as a downstream effector of the BMP signaling pathway. (C) 2004 Elsevier Inc. All rights reserved.