Human amyloid precursor protein ameliorates behavioral deficit of flies deleted for Appl gene

Neuron. 1992 Oct;9(4):595-605. doi: 10.1016/0896-6273(92)90024-8.


Drosophila amyloid precursor protein-like (Appl) gene encodes a protein product (APPL) similar to beta-amyloid precursor protein (APP) associated with Alzheimer's disease. To understand the in vivo function of APPL protein, we have generated flies deleted for the Appl gene. These flies are viable, fertile, and morphologically normal, yet they exhibit subtle behavioral deficits. We show that a fast phototaxis defect in Appl- flies is partially rescued by transgenes expressing the wild-type, but not a mutant, APPL protein. We further demonstrate a functional homology between APPL and APP, since transgenes expressing human APP show a similar level of rescue as transgenes expressing fly APPL.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amyloid beta-Protein Precursor / analysis
  • Amyloid beta-Protein Precursor / genetics*
  • Amyloid beta-Protein Precursor / physiology*
  • Animals
  • Animals, Genetically Modified
  • Blotting, Western
  • Chromosome Mapping
  • Crosses, Genetic
  • DNA / genetics
  • Drosophila melanogaster / genetics
  • Drosophila melanogaster / physiology*
  • Female
  • Gene Deletion*
  • Genotype
  • Heat-Shock Proteins / analysis
  • Heat-Shock Proteins / genetics*
  • Humans
  • Light
  • Male
  • Motor Activity*
  • Recombinant Fusion Proteins / analysis
  • X Chromosome
  • Y Chromosome


  • Amyloid beta-Protein Precursor
  • Heat-Shock Proteins
  • Recombinant Fusion Proteins
  • DNA