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Invest Ophthalmol Vis Sci. 2005 Jan;46(1):12-6.

GC1 deletion prevents light-dependent arrestin translocation in mouse cone photoreceptor cells.

Author information

Department of Neuroscience, McKnight Brain Institute and College of Medicine, University of Florida, Gainesville, Florida 32610-0255, USA.

Erratum in

  • Invest Ophthalmol Vis Sci. 2005 Feb;46(2):414.



Light-driven translocation of phototransduction regulatory proteins between the inner and outer segments of photoreceptor cells plays a role in the adaptation of these cells to light. The purpose of this study was to examine the effects of the absence of guanylate cyclase 1 (GC1) on light-driven protein translocation in rod and cone cells. Both cell types express GC1, but differ in sensitivity, saturation, and response times to light.


Immunohistochemical techniques employing antibodies specific for cone and rod transducin alpha (Talpha) subunits and arrestins were used to examine light-driven translocation of these proteins in the retinas of wild-type and GC1 knockout (KO) mice.


Translocation of cone arrestin from cone outer segments to the inner cell regions was disrupted in the absence of GC1, whereas translocation of arrestin and Talpha in rods was not affected. Cone Talpha did not translocate in wild-type and GC1 KO mice, but differed in its subcellular distribution in GC1 KO retina, remaining in the cone outer segment in light and in dark.


These results suggest that multiple, independent pathways regulate the translocation of phototransduction proteins and that GC1, and presumably cGMP, are of key importance in signaling the translocation of cone arrestin.

[Indexed for MEDLINE]

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