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Related Experiment Video

Updated: Jun 19, 2026

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

Published on: April 6, 2022

The evolution of senescence in multi-component systems.

Robert A Laird¹, Thomas N Sherratt

¹Department of Biology, Carleton University, Ottawa, Ontario, Canada. robert.laird@uleth.ca

|November 3, 2009

Summary

This study introduces a discrete-time reliability theory of senescence, showing that redundancy drives aging in parallel and cascade models. Evolution predicts increasing redundancy limited by mutation-selection balance.

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Area of Science:

Evolutionary biology
Gerontology
Theoretical biology

Background:

Actuarial senescence, an increase in mortality with age, is a fundamental biological phenomenon.
The reliability theory of senescence models vital functions as damageable elements, where survival depends on at least one element remaining intact.
Existing reliability models are continuous-time and lack an evolutionary component.

Purpose of the Study:

To develop a discrete-time version of the reliability theory of senescence incorporating evolutionary dynamics.
To investigate the role of redundancy in actuarial senescence across different model structures (Series, Parallel, Cascade).
To predict the evolutionary trajectory of redundancy and senescence under mutation-selection balance.

Main Methods:

Derivation of a discrete-time reliability theory of senescence using probability theory and evolutionary dynamics analysis.
Modeling three variations: Series (any damage causes death), Parallel (all damage causes death), and Cascade (sequential damage causes death).
Analysis using the discrete-generation quasispecies equation to model evolutionary dynamics.

Main Results:

Redundancy leads to actuarial senescence in Parallel and Cascade models, but not in the Series model.
Lifetime reproductive output is a positive, decelerating function of redundancy in Parallel and Cascade models.
Evolutionary dynamics confirm that redundancy and senescence evolve from non-senescing ancestors, with increased redundancy limited by mutation-selection balance.
Equilibrium redundancy is sensitive to extrinsic mortality rates.

Conclusions:

Redundancy is a key driver of actuarial senescence under specific biological architectures (Parallel, Cascade).
Evolution favors increased redundancy, but this process is constrained by mutation-selection balance.
Environmental factors, like extrinsic mortality, influence the evolution of redundancy and aging.