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Heads‐up: New roles for the fragile X mental retardation protein in neural stem and progenitor cells
Author(s) -
Callan Matthew A.,
Zarnescu Daniela C.
Publication year - 2011
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20745
Subject(s) - fragile x syndrome , neurogenesis , neurosphere , neural stem cell , progenitor cell , biology , embryonic stem cell , neuroscience , fragile x , progenitor , stem cell , fmr1 , neural development , translation (biology) , nervous system , adult stem cell , microbiology and biotechnology , genetics , gene , messenger rna
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. © 2011 Wiley‐Liss, Inc.