PUBLICATION

Characterization of dFMR1, a Drosophila melanogaster homolog of the fragile X mental retardation protein

Authors
Wan, L., Dockendorff, T.C., Jongens, T.A., and Dreyfuss, G.
ID
ZDB-PUB-020806-1
Date
2000
Source
Molecular and cellular biology   20(22): 8536-8547 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Amino Acid Motifs
  • Amino Acid Sequence
  • Amino Acid Substitution
  • Animals
  • Antibodies, Monoclonal
  • Apoptosis/genetics
  • Cloning, Molecular
  • Drosophila melanogaster/embryology
  • Drosophila melanogaster/genetics*
  • Embryo, Nonmammalian
  • Fragile X Mental Retardation Protein
  • Gene Expression Regulation, Developmental
  • Genes, Dominant
  • Insect Proteins/genetics*
  • Insect Proteins/immunology
  • Insect Proteins/metabolism*
  • Molecular Sequence Data
  • Nerve Tissue Proteins/genetics*
  • Nerve Tissue Proteins/immunology
  • Nerve Tissue Proteins/metabolism
  • RNA/metabolism
  • RNA-Binding Proteins*
  • Sequence Homology, Amino Acid
PubMed
11046149 Full text @ Mol. Cell. Biol.
Abstract
Fragile X syndrome is the most common inherited form of mental retardation. It is caused by loss of FMR1 gene activity due to either lack of expression or expression of a mutant form of the protein. In mammals, FMR1 is a member of a small protein family that consists of FMR1, FXR1, and FXR2. All three members bind RNA and contain sequence motifs that are commonly found in RNA-binding proteins, including two KH domains and an RGG box. The FMR1/FXR proteins also contain a 60S ribosomal subunit interaction domain and a protein-protein interaction domain which mediates homomer and heteromer formation with each family member. Nevertheless, the specific molecular functions of FMR1/FXR proteins are unknown. Here we report the cloning and characterization of a Drosophila melanogaster homolog of the mammalian FMR1/FXR gene family. This first invertebrate homolog, termed dfmr1, has a high degree of amino acid sequence identity/similarity with the defined functional domains of the FMR1/FXR proteins. The dfmr1 product binds RNA and is similar in subcellular localization and embryonic expression pattern to the mammalian FMR1/FXR proteins. Overexpression of dfmr1 driven by the UAS-GAL4 system leads to apoptotic cell loss in all adult Drosophila tissues examined. This phenotype is dependent on the activity of the KH domains. The ability to induce a dominant phenotype by overexpressing dfmr1 opens the possibility of using genetic approaches in Drosophila to identify the pathways in which the FMR1/FXR proteins function.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping