Sunrise at the synapse: the FMRP mRNP shaping the synaptic interface

Neuron. 2003 Feb 20;37(4):555-8. doi: 10.1016/s0896-6273(03)00090-4.


Recent studies provide new insight into the mechanistic function of Fragile X Mental Retardation Protein (FMRP), paving the way to understanding the biological basis of Fragile X Syndrome. While it has been known for several years that there are spine defects associated with the absence of the mRNA binding protein FMRP, it has been unclear how its absence may lead to specific synaptic defects that underlie the learning and cognitive impairments in Fragile X. One hypothesis under study is that FMRP may play a key role in the regulation of dendritically localized mRNAs, at subsynaptic sites where regulation of local protein synthesis may influence synaptic structure and plasticity. This review highlights recent progress to identify the specific mRNA targets of FMRP and assess defects in mRNA regulation that occur in cells lacking FMRP. In addition, exciting new studies on Fmr1 knockout mice and mutant flies have begun to elucidate a key role for FMRP in synaptic growth, structure, and long-term plasticity.

Publication types

  • Review

MeSH terms

  • Animals
  • Biological Transport
  • Fragile X Mental Retardation Protein
  • Fragile X Syndrome / metabolism*
  • Humans
  • Mice
  • Mice, Knockout
  • Nerve Tissue Proteins / metabolism*
  • Neuronal Plasticity / physiology
  • Protein Binding / physiology
  • Protein Biosynthesis / physiology
  • RNA, Messenger / metabolism*
  • RNA-Binding Proteins*
  • Ribonucleoproteins / metabolism*
  • Synapses / metabolism*


  • FMR1 protein, human
  • Fmr1 protein, mouse
  • Nerve Tissue Proteins
  • RNA, Messenger
  • RNA-Binding Proteins
  • Ribonucleoproteins
  • messenger ribonucleoprotein
  • Fragile X Mental Retardation Protein