Hypotheses on the extended phenotype of the mitochondrion: sex, mortality, and aging

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Authors

Gordon Irlam

Abstract

How did sex evolve, how is sex evolutionary stable, and why do eukaryotes appear mortal. This paper presents a mitochondrial perspective on the evolution of the eukaryotic cell that appears capable of answering these questions. Rather than viewing a mitochondrion as a passive entity taken up by an archaeal host that remains in the driving seat, mitochondria are viewed as the key force driving eukaryogenesis. The proto-mitochondrion is presumed to have manipulated its archaeal host to engage in sex in order to replicate itself in a more and more beneficial environment. This process is hypothesized to still be operating today as a result of the mitochondrion’s continued production of reactive oxygen species (ROS). The specific production of ROS by the mitochondrion appears to be an intentional mechanism to cause the organism ultimately to die. Faced with mortality, if the organism wishes to pass on its nuclear genes it will typically engage in sex as a means of resetting age. Eukaryotic species that instead reproduced parthenogenetically would find themselves out-competed by sexual species due to the reassortment of genes that comes with sex. The species benefits from a shortened time between successive sexual generations which creates an increased ability to adapt to a changing environment.

DOI

https://doi.org/10.32942/X2H309

Subjects

Biology, Evolution

Keywords

evolution, Eukaryogenesis, extended phenotype, mitochondria, sex, Mortality, aging, reactive oxygen species, cellular senescence, age-related diseases

Dates

Published: 2023-06-19 02:29

Last Updated: 2024-04-11 12:50

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License

CC-By Attribution-ShareAlike 4.0 International

Additional Metadata

Language:
English

Conflict of interest statement:
None

Data and Code Availability Statement:
Data: https://doi.org/10.5281/zenodo.7901578 Code: https:/doi.org/10.5281/zenodo.7901622