Loss of the phospholipase C gene product induces massive endocytosis of rhodopsin and arrestin in Drosophila photoreceptors

Vision Res. 2002 Feb;42(4):497-505. doi: 10.1016/s0042-6989(01)00229-2.

Abstract

Previously we have shown that a subset of visual transduction mutants in Drosophila melanogaster induce the formation of stable complexes between rhodopsin and arrestin. One such mutant is in a visual system-specific phospholipase C (PLC). The rhodopsin/arrestin complexes generated in PLC mutants induce massive retinal degeneration. Here we demonstrate that both arrestin and rhodopsin undergo light-dependent endocytosis in a PLC mutant background. Interestingly, the internalized rhodopsin is rapidly degraded, but the arrestin is fully stable. The data are discussed with respect to mechanisms of arrestin-mediated endocytosis and human retinal disease.

Publication types

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

MeSH terms

  • Animals
  • Arrestin / metabolism*
  • Drosophila melanogaster
  • Endocytosis*
  • Immunohistochemistry
  • Microscopy, Confocal
  • Models, Animal
  • Phosphatidylinositol Diacylglycerol-Lyase
  • Photoreceptor Cells, Invertebrate / metabolism*
  • Retinitis Pigmentosa / metabolism*
  • Rhodopsin / metabolism*
  • Type C Phospholipases / metabolism*

Substances

  • Arrestin
  • Rhodopsin
  • Type C Phospholipases
  • Phosphatidylinositol Diacylglycerol-Lyase