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The formation of stable rhodopsin-arrestin complexes induces apoptosis and photoreceptor cell degeneration.

Although many different mutations in humans and Drosophila cause retinal degeneration, in most cases, a molecular mechanism for the degeneration has not been found. We now demonstrate the existence of stable, persistent complexes between rhodopsin and its regulatory protein arrestin in several different retinal degeneration mutants. Elimination of these rhodopsin-arrestin complexes by removing either rhodopsin or arrestin rescues the degeneration phenotype. Furthermore, we show that the accumulation of these complexes triggers apoptotic cell death and that the observed retinal degeneration requires the endocytic machinery. This suggests that the endocytosis of rhodopsin-arrestin complexes is a molecular mechanism for the initiation of retinal degeneration. We propose that an identical mechanism may be responsible for the pathology found in a subset of human retinal degenerative disorders.

Pubmed ID: 11086989


  • Alloway PG
  • Howard L
  • Dolph PJ



Publication Data

October 21, 2000

Associated Grants

  • Agency: NEI NIH HHS, Id: R01 EY11534-02

Mesh Terms

  • Animals
  • Apoptosis
  • Arrestin
  • Arrestins
  • Drosophila
  • Drosophila Proteins
  • Endocytosis
  • Eye Proteins
  • Light
  • Membrane Proteins
  • Mutation
  • Phosphatidylinositol Diacylglycerol-Lyase
  • Phosphoproteins
  • Phosphorylation
  • Photoreceptor Cells, Invertebrate
  • Retinal Degeneration
  • Rhodopsin
  • Type C Phospholipases