Heads-Up: New Roles for the Fragile X Mental Retardation Protein in Neural Stem and Progenitor Cells

被引:33
作者
Callan, Matthew A. [1 ]
Zarnescu, Daniela C. [1 ,2 ,3 ]
机构
[1] Univ Arizona, Dept Mol & Cellular Biol, Tucson, AZ 85721 USA
[2] Univ Arizona, Dept Neurosci, Tucson, AZ 85721 USA
[3] Univ Arizona, Dept Neurol, Tucson, AZ 85721 USA
基金
美国国家卫生研究院;
关键词
fate specification; neural tissue; proliferation; differentiation; neurogenesis; fragile X syndrome; CENTRAL-NERVOUS-SYSTEM; FMR1 KNOCKOUT MICE; MESSENGER-RNA TRANSPORT; DROSOPHILA-MELANOGASTER; MOUSE MODEL; GENE-EXPRESSION; DENDRITIC SPINES; IN-VIVO; POSTEMBRYONIC NEUROBLASTS; SYNAPTIC PLASTICITY;
D O I
10.1002/dvg.20745
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Fragile X syndrome (FXS) is the most common form of inherited mental retardation and is caused by the loss of function for Fragile X Mental Retardation Protein (FMRP), a selective RNA-binding protein with a demonstrated role in the localized translation of target mRNAs at synapses. Several recent studies provide compelling evidence for a new role of FMRP in the development of the nervous system, during neurogenesis. Using a multi-faceted approach and a variety of model systems ranging from cultured neurospheres and progenitor cells to in vivo Drosophila and mouse models these reports indicate that FMRP is required for neural stem and progenitor cell proliferation, differentiation, survival, as well as regulation of gene expression. Here we compare and contrast these recent reports and discuss the implications of FMRP's new role in embryonic and adult neurogenesis, including the development of novel therapeutic approaches to FXS and related neurological disorders such as autism. genesis 49:424-440, 2011. (C) 2011 Wiley-Liss, Inc.
引用
收藏
页码:424 / 440
页数:17
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