Age (Dordrecht, Netherlands)Dec 30, 2011

Faster protein changes identify genes and pathways linked to longer mammal lifespans

Updated Feb 11, 2026

Abstract

Proteins related to longevity-specific selection patterns were identified, including COL3A1, DDB1, and CAPNS1.

Analysis of proteins in mammalian lineages with increased maximum lifespan revealed candidate genes and processes linked to longevity evolution.
Several proteins related to DNA damage repair and response showed selection patterns associated with longevity.
Processes involved in lipid metabolism and cholesterol breakdown were identified as potentially linked to the evolution of longevity.
Evidence suggests that the proteasome-ubiquitin system is under selection in species with increased longevity.

Simplified

The genetic basis of the large species differences in longevity and aging remains a mystery. Thanks to recent large-scale genome sequencing efforts, the genomes of multiple species have been sequenced and can be used for cross-species comparisons to study species divergence in longevity. By analyzing proteins under accelerated evolution in several mammalian lineages where maximum lifespan increased, we identified genes and processes that are candidate targets of selection when longevity evolves. We identified several proteins with longevity-specific selection patterns, including COL3A1 that has previously been related to aging and proteins related to DNA damage repair and response such as DDB1 and CAPNS1. Moreover, we found that processes such as lipid metabolism and cholesterol catabolism show such patterns of selection and suggest a link between the evolution of lipid metabolism, cholesterol catabolism, and the evolution of longevity. Lastly, we found evidence that the proteasome-ubiquitin system is under selection specific to lineages where longevity increased and suggest that its selection had a role in the evolution of longevity. These results provide evidence that natural selection acts on species when longevity evolves, give insights into adaptive genetic changes associated with the evolution of longevity in mammals, and provide evidence that at least some repair systems are selected for when longevity increases.

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