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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

This summary is machine-generated.

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.

Keywords:

Muller’s ratchet aging fitness decay frailty morbidity mutation accumulation senescence somatic cell lineages

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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.