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Published on: September 29, 2011
A model for damage load and its implications for the evolution of bacterial aging
1Section of Ecology, Behavior, and Evolution, Division of Biological Sciences, University of California San Diego, La Jolla, California, United States of America. LChao@ucsd.edu
Harmful non-heritable damage creates a "damage load," impacting fitness and favoring asymmetrical inheritance, which can lead to aging. Symmetrical cell division offers immortality below a damage threshold, while asymmetry allows persistence above it.
Area of Science:
- Evolutionary Biology
- Genetics
- Cell Biology
Background:
- Deleterious mutations accumulate until natural selection halts them, creating a mutational load.
- Harmful non-heritable phenotypic changes can also accumulate, forming a comparable 'damage load'.
Purpose of the Study:
- To introduce and define the concept of a damage load.
- To explore the evolutionary implications of damage load, including its effect on inheritance asymmetry and aging.
- To model the relationship between damage load, inheritance asymmetry, and organismal lifespan.
Main Methods:
- Development of a mathematical model based on microbial cell division.
- Analysis of symmetrical versus asymmetrical damage transmission.
- Fitting the model to experimental data from Escherichia coli.
Main Results:
- A damage load favors asymmetrical transmission of damage from mother to daughter cells.
- Symmetrical division leads to immortality if damage rates are below a threshold; asymmetry allows survival above this threshold but results in mortality.
- Escherichia coli exhibits a damage rate below the immortality threshold and possesses low asymmetry, suggesting a trade-off between fitness returns and asymmetry.
Conclusions:
- The damage load is a significant factor in evolutionary biology, comparable to the mutational load.
- Asymmetrical damage transmission, while potentially increasing fitness variance and enabling survival at higher damage rates, is linked to aging and mortality.
- Microbial models suggest that the damage load can exceed the mutational load, and evolutionary pressures shape asymmetry levels for optimal persistence.
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