The Journal of Neuroscience, January 18, 2006, ():
Deactivation of Phosphorylated and Nonphosphorylated Rhodopsin by Arrestin Splice Variants
J. Neurosci. Burns et al.
26: 1036
Supplemental data
Files in this Data Supplement:
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Supplemental Figure S1. Pathways for R* deactivation. Upon activation by a photon (hν), rhodopsin (R) undergoes a conformational change to the most catalytically-active form, metarhodopsin II (R*), which then drives the light response. In a normal rod, phosphorylation by RK (R*-P) reduces this catalytic activity, with complete deactivation occurring only upon subsequent arrestin binding (Xu et al., 1997; RP-Arr). In normal rods, this complete deactivation of R* occurs within 200 ms or less, the time constant of recovery of wild type photoresponses. In the absence of phosphorylation, reversible deactivation of R* occurs on a time scale of ~5 s and is facilitated by p48 arrestin (R-Arr). In the absence of arrestin, the activities of R* and R*-P are ultimately quenched by a process requiring many tens of seconds, which likely reflects thermal decay to free opsin.
