细胞生物学
神经褶
神经板
颅神经嵴
心脏发育
丛蛋白
神经发育
形态发生
欧米林
神经管
中胚层
间充质
神经系统
神经发生
作者
Christopher B. Brown,Leonard Feiner,Minmin Lu,Jun Li,Xiaokui Ma,Andrea L. Webber,Li Jia,Jonathan A. Raper,Jonathan A. Epstein
出处
期刊:Development
[The Company of Biologists]
日期:2001-08-15
卷期号:128 (16): 3071-3080
被引量:195
标识
DOI:10.1242/dev.128.16.3071
摘要
Classic studies using avian model systems have demonstrated that cardiac neural crest cells are required for proper development of the cardiovascular system. Environmental influences that perturb neural crest development cause congenital heart defects in laboratory animals and in man. However, little progress has been made in determining molecular programs specifically regulating cardiac neural crest migration and function. Only recently have complex transgenic tools become available that confirm the presence of cardiac neural crest cells in the mammalian heart. These studies have relied upon the use of transgenic mouse lines and fate-mapping studies using Cre recombinase and neural crest-specific promoters. In this study, we use these techniques to demonstrate that PlexinA2 is expressed by migrating and postmigratory cardiac neural crest cells in the mouse. Plexins function as co-receptors for semaphorin signaling molecules and mediate axon pathfinding in the central nervous system. We demonstrate that PlexinA2-expressing cardiac neural crest cells are patterned abnormally in several mutant mouse lines with congenital heart disease including those lacking the secreted signaling molecule Semaphorin 3C. These data suggest a parallel between the function of semaphorin signaling in the central nervous system and in the patterning of cardiac neural crest in the periphery.
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