Loss of the phospholipase C gene product induces massive endocytosis of rhodopsin and arrestin in Drosophila photoreceptors.
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.
Orem
Nicholas R
NR
Department of Biological Sciences, Dartmouth College, 6044 Gilman, Hanover, NH 03755, USA.
Dolph
Patrick J
PJ
D000818:Animals; D019393:Arrestin / Q000378:metabolism*; D004331:Drosophila melanogaster; D004705:Endocytosis; D007150:Immunohistochemistry; D018613:Microscopy, Confocal; D023421:Models, Animal; D043265:Phosphatidylinositol Diacylglycerol-Lyase; D017956:Photoreceptor Cells, Invertebrate / Q000378:metabolism*; D012174:Retinitis Pigmentosa / Q000378:metabolism*; D012243:Rhodopsin / Q000378:metabolism*; D010738:Type C Phospholipases / Q000378:metabolism*
D019393:Arrestin; D012243:Rhodopsin; D010738:Type C Phospholipases; D043265:Phosphatidylinositol Diacylglycerol-Lyase