This study investigates the effects of reduced translational fidelity on aging by introducing a D95N point mutation in the ribosomal protein S9 (Rps9) gene in mice. The Rps9 D95N Knockin mice exhibit genome-wide error-prone translation, leading to a reduced lifespan and early onset of aging-related phenotypes, including physical deformities, poor fur condition, lymphopenia, increased oxidative damage, accelerated DNA methylation changes, and telomere attrition. These findings establish a causal link between translational accuracy and aging in mammals.
The Rps9 D95N mutation induces error-prone protein synthesis, resulting in premature aging phenotypes and reduced lifespan, highlighting the importance of translational fidelity in aging.
Rps9 D95N Knockin mouse model generated to assess the impact of translational errors on aging processes.
Aging, Translational fidelity, Ribosomal function, Oxidative stress, Epigenetic changes
Knockin model, Point mutation, Ribosomal ambiguity mutation, Protein synthesis accuracy
From model design to experimental results
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Models with certified health status from professional breeders in US and Europe
