From fragile X mental retardation protein to Rac1 GTPase: new insights from Fly CYFIP

Neuron. 2003 Jun 19;38(6):843-5. doi: 10.1016/s0896-6273(03)00362-3.

Abstract

Mutations in either the Rho GTPase pathway or in the fragile X mental retardation (FMR1) gene produce neuronal connectivity defects. In this issue of Neuron, Schenck et al. use biochemical and genetic approaches in Drosophila to examine the interactions between dFMR1 and dRac1 and provide evidence that the cytoplasmic FMRP interacting protein (CYFIP) links Rac-dependent cytoskeleton remodeling and dFMR1-dependent control of translation in a unique pathway to modulate neuronal morphogenesis.

Publication types

  • Comment

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Animals
  • Carrier Proteins / genetics
  • Carrier Proteins / physiology*
  • Drosophila Proteins*
  • Drosophila melanogaster* / genetics
  • Fragile X Mental Retardation Protein
  • Humans
  • Intellectual Disability / genetics
  • Mutation
  • Nerve Tissue Proteins* / genetics
  • Neurons / ultrastructure*
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / physiology
  • rac GTP-Binding Proteins / genetics
  • rac GTP-Binding Proteins / physiology
  • rac1 GTP-Binding Protein*

Substances

  • Adaptor Proteins, Signal Transducing
  • CYFIP1 protein, human
  • Carrier Proteins
  • Drosophila Proteins
  • FMR1 protein, Drosophila
  • FMR1 protein, human
  • Nerve Tissue Proteins
  • RNA-Binding Proteins
  • Rac1 protein, Drosophila
  • Sra-1 protein, Drosophila
  • Fragile X Mental Retardation Protein
  • rac GTP-Binding Proteins
  • rac1 GTP-Binding Protein