| First Author | Song X | Year | 2011 |
| Journal | Neuroscience | Volume | 174 |
| Pages | 37-49 | PubMed ID | 21075174 |
| Mgi Jnum | J:170273 | Mgi Id | MGI:4946166 |
| Doi | 10.1016/j.neuroscience.2010.11.009 | Citation | Song X, et al. (2011) Arrestin-1 expression level in rods: balancing functional performance and photoreceptor health. Neuroscience 174:37-49 |
| abstractText | In rod photoreceptors, signaling persists as long as rhodopsin remains catalytically active. Phosphorylation by rhodopsin kinase followed by arrestin-1 binding completely deactivates rhodopsin. Timely termination prevents excessive signaling and ensures rapid recovery. Mouse rods express arrestin-1 and rhodopsin at approximately 0.8:1 ratio, making arrestin-1 the second most abundant protein in the rod. The biological significance of wild type arrestin-1 expression level remains unclear. Here we investigated the effects of varying arrestin-1 expression on its intracellular distribution in dark-adapted photoreceptors, rod functional performance, recovery kinetics, and morphology. We found that rod outer segments isolated from dark-adapted animals expressing arrestin-1 at wild type or higher level contain much greater fraction of arrestin-1 than previously estimated, 15-25% of the total. The fraction of arrestin-1 residing in the outer segments (OS) in animals with low expression (4-12% of wild type) is much lower, 5-7% of the total. Only 4% of wild type arrestin-1 level in the outer segments was sufficient to maintain near-normal retinal morphology, whereas rapid recovery required at least approximately 12%. Supra-physiological arrestin-1 expression improved light sensitivity and facilitated photoresponse recovery, but was detrimental for photoreceptor health, particularly in the peripheral retina. Thus, physiological level of arrestin-1 expression in rods reflects the balance between short-term functional performance of photoreceptors and their long-term health. |
