Members of the arrestin superfamily have great propensity of self-association, but the physiological significance of this phenomenon is unclear. To determine the biological role of visual arrestin-1 oligomerization in rod photoreceptors, we expressed mutant arrestin-1 with severely impaired self-association in mouse rods and analyzed mice of both sexes. We show that the oligomerization-deficient mutant is capable of quenching rhodopsin signaling normally, as judged by electroretinography and single-cell recording. Like wild type, mutant arrestin-1 is largely excluded from the outer segments in the dark, proving that the normal intracellular localization is not due the size exclusion of arrestin-1 oligomers. In contrast to wild type, supraphysiological expression of the mutant causes shortening of the outer segments and photoreceptor death. Thus, oligomerization reduces the cytotoxicity of arrestin-1 monomer, ensuring long-term photoreceptor survival.
750 outer segments measured per genotype. A normal Gaussian distribution was fit to each genotype. Unpaired, two-tailed t-test (assuming equal variances) t-test was performed to assess any statistical differences between genotypes. To determine the total rhodopsin content of eyecups, difference spectra were taken from each of three dissected eyecups per genotype. Unpaired, two-tailed t-test (assuming equal variances) was performed to assess any statistical differences between genotypes. To quantify outer segment length, the lengths of outer segments in five regions across the retina were measured of each of three different retinal sections per genotype. Unpaired, two-tailed t-test (assuming equal variances) was performed to assess any statistical differences between genotypes. For all experiments, significance is labeled as *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001. Non-significant values are unlabeled. Data is represented as mean ± standard error of the mean.
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