The evolution of senescence through decelerating selection for system reliability.

Area of Science:

• Evolutionary Biology
• Gerontology
• Genetics

Background:

• Senescence, characterized by increased mortality and decreased fecundity with age, is a universal biological phenomenon.
• Proximate causes of senescence, like oxidative stress, involve bodily damage, but evolutionary theories often focus on detrimental gene effects.
• A gap exists between proximate damage-based explanations and ultimate evolutionary theories of senescence.

Purpose of the Study:

• To present a novel evolutionary model of senescence based on reliability theory.
• To explain senescence as a consequence of gradual damage and failure of essential gene products, rather than active harm from functioning genes.
• To investigate how redundancy in gene products evolves in response to environmental factors and genetic damage.

Main Methods:

• Development of an evolutionary model using reliability theory.
• Modeling the evolution of redundant gene copies for vital functions, where survival depends on at least one functional copy.
• Analysis of mutation-selection balance to determine population-level distributions of redundancy.

Main Results:

• Organisms with lower extrinsic mortality and higher genetic damage levels evolve greater redundancy.
• Mutation-selection balance leads to stable population distributions of redundant elements.
• The model's emergent mortality curves match empirical senescence patterns: increasing mortality at young ages, a plateau in advanced ages, and mortality compensation.

Conclusions:

• Senescence can be explained by the accumulation of damage to essential gene products, leading to their failure.
• The evolution of redundancy provides a mechanism for organisms to cope with inevitable genetic damage over time.
• This reliability theory-based model successfully replicates key empirical features of aging and mortality across different environmental conditions.