Premature aging in mice with error-prone protein synthesis

Dimitri Shcherbakov
Universität Zürich
April 1, 2022
Sci Adv
https://pubmed.ncbi.nlm.nih.gov/35235349

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/35235349

Research summary

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.

Key outcome of the study

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.

Mouse model

Rps9 D95N Knockin mouse model generated to assess the impact of translational errors on aging processes.

TARGET:
Rps9
Ribosomal protein S9

Keywords

Aging, Translational fidelity, Ribosomal function, Oxidative stress, Epigenetic changes

Technical specifications

Knockin model, Point mutation, Ribosomal ambiguity mutation, Protein synthesis accuracy

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