ArticleFrontiers in molecular neuroscience2018
Enhanced Mutant Compensates for Defects in Rhodopsin Phosphorylation in the Presence of Endogenous Arrestin-1.
Article in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- The role of arrestin-1 N-edge in rhodopsin binding.Cellular signalling · 2025Article
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- Modulating signalling lifetime to optimise a prototypical animal opsin for optogenetic applications.Pflugers Archiv : European journal of physiology · 2023Article
- Review
- The Role of Arrestin-1 Middle Loop in Rhodopsin Binding.International journal of molecular sciences · 2022Article
- Solo vs. Chorus: Monomers and Oligomers of Arrestin Proteins.International journal of molecular sciences · 2022Review
- Arrestin Facilitates Rhodopsin DephosphorylationThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Targeting arrestin interactions with its partners for therapeutic purposes.Advances in protein chemistry and structural biology · 2020Review
- Article
- GPCR Signaling Regulation: The Role of GRKs and Arrestins.Frontiers in pharmacology · 2019Review
- Arrestin mutations: Some cause diseases, others promise cure.Progress in molecular biology and translational science · 2019Review
- Arrestins: Introducing Signaling Bias Into Multifunctional Proteins.Progress in molecular biology and translational science · 2018Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
We determined the effects of different expression levels of arrestin-1-3A mutant with enhanced binding to light-activated rhodopsin that is independent of phosphorylation. To this end, transgenic mice that express mutant rhodopsin with zero, one, or two phosphorylation sites, instead of six in the WT mouse rhodopsin, and normal complement of WT arrestin-1, were bred with mice expressing enhanced phosphorylation-independent arrestin-1-3A mutant. The resulting lines were characterized by retinal histology (thickness of the outer nuclear layer, reflecting the number of rod photoreceptors, and the length of the outer segments, which reflects rod health), as well as single- and double-flash ERG to determine the functionality of rods and the rate of photoresponse recovery. The effect of co-expression of enhanced arrestin-1-3A mutant with WT arrestin-1 in these lines depended on its level: higher (240% of WT) expression reduced the thickness of ONL and the length of OS, whereas lower (50% of WT) expression was harmless in the retinas expressing rhodopsin with zero or one phosphorylation site, and improved photoreceptor morphology in animals expressing rhodopsin with two phosphorylation sites. Neither expression level increased the amplitude of the a- and b-wave of the photoresponse in any of the lines. However, high expression of enhanced arrestin-1-3A mutant facilitated photoresponse recovery 2-3-fold, whereas lower level was ineffective. Thus, in the presence of normal complement of WT arrestin-1 only supra-physiological expression of enhanced mutant is sufficient to compensate for the defects of rhodopsin phosphorylation.
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