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The Muller's Ratchet and Aging
Diddahally R Govindaraju1, Hideki Innan2, Reiner A Veitia3
1Museum of Comparative Zoology, Harvard University, Cambridge, MA 02138, USA; Institute of Aging Research, Albert Einstein College of Medicine, Bronx, NY 10460, USA.
Trends in Genetics : TIG
|May 13, 2020
Summary
Aging involves irreversible physiological decline due to accumulated genetic and epigenetic alterations. This study revisits Muller's ratchet to explain cellular aging, senescence, and morbidity.
Area of Science:
- Gerontology
- Molecular Biology
- Genetics
Background:
- Aging is characterized by physiological decline and reduced tissue integrity.
- Accumulation of genetic and epigenetic alterations is a proposed cause of aging.
- Cell division errors contribute to deleterious molecular changes.
Purpose of the Study:
- To revisit the Muller's ratchet principle in the context of somatic cell aging.
- To explore the implications of accumulated alterations for cellular fitness.
- To discuss the origins of senescence, frailty, and morbidity.
Main Methods:
- Revisiting the Muller's ratchet principle.
- Applying the principle to somatic cell populations.
- Discussing implications for aging-related conditions.
Main Results:
- Deleterious genetic and epigenetic alterations accumulate irreversibly.
- This accumulation reduces cellular fitness, akin to Muller's ratchet.
- The process explains stepwise decline in cellular function.
Conclusions:
- Muller's ratchet provides a framework for understanding somatic cell aging.
- Accumulated alterations are key drivers of senescence and frailty.
- This perspective aids in understanding the origins of age-related diseases.
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