Heads-up: New roles for the fragile X mental retardation protein in neural stem and progenitor cells

Matthew A. Callan, Daniela C. Zarnescu

Research output: Contribution to journalReview articlepeer-review

37 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)424-440
Number of pages17
Issue number6
StatePublished - Jun 2011


  • Differentiation
  • Fate specification
  • Fragile X syndrome
  • Neural tissue
  • Neurogenesis
  • Proliferation

ASJC Scopus subject areas

  • Genetics
  • Endocrinology
  • Cell Biology


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