First published online July 25, 2006
Journal of Cell Science 119, 1504e (2006)
© The Company of Biologists Limited
... and is a sight for sore eyes
Inherited retinal diseases are characterized by late-onset, progressive loss of photoreceptor cells. Some of the mechanisms underlying these diseases have been identified in studies of the Drosophila visual system. Now, Patrick Dolph and colleagues report that an interaction between a visual arrestin - Arr2 - and the endocytic adapter protein AP-2 is required for the physiological and pathological endocytosis of rhodopsin in Drosophila photoreceptor cells (see p. 3141). The visual transduction cascade is partly regulated by inactivation of rhodopsin after the photoreceptor cell has been depolarized. This involves a transient interaction between Arr2 and rhodopsin. In Drosophila norpA mutants, by contrast, the complexes persist and kill the photoreceptors through extensive endocytosis. The authors show that endocytosis requires an AP-2-interaction motif in Arr2 and that disruption of the Arr2-AP-2 interaction prevents norpA-induced retinal degeneration. Blocking the Arr2-AP-2 interaction in normal photoreceptors also causes retinal degeneration, however. Thus, Arr2-AP-2-mediated endocytosis maintains healthy photoreceptors by facilitating rhodopsin turnover but is also required for pathological endocytosis-mediated photoreceptor cell death.
Related articles in JCS:
- An essential role for endocytosis of rhodopsin through interaction of visual arrestin with the AP-2 adaptor
- Nicholas R. Orem, Luxi Xia, and Patrick J. Dolph
JCS 2006 119: 3141-3148.
[Abstract]
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