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Aging May Be As Old As Life Itself

Summary: Researchers report that, at the molecular levels, aging may have originated at the beginning of the evolution of life. They suggest when it comes to genes, aging may not always be a negative trait, and may help an organism to survive.

Source: USC.

A new USC Dornsife study indicates that aging may have originated at the very beginning of the evolution of life, at the same time as the evolution of the first genes.

“This could be a game changer for research on longevity and aging. It may also be relevant to the scientific discussions surrounding CRISPR9 gene editing,” said John Tower, biologist at the USC Dornsife College of Letters, Arts and Sciences. “We found that when it comes to genes, aging may not always be a negative trait. It may help an organism survive.”

The findings, published on Sept. 11 in the journal Origins of Life and Evolution and Biospheres, may reshape scientific conversations about a long-held hypothesis of aging first proposed by the biologist George C. Williams.

Williams had suggested in a 1957 paper that as part of natural selection, biology favors genes that will optimize functions and characteristics necessary for reproduction within a specific period of time. But later in life, those genes that enhance reproduction actually contribute to aging. Williams’ hypothesis was known as “antagonistic pleiotropy.”

There are several examples of this biological tradeoff. The gene p53, for example, suppresses cancer, but it is known to accelerate aging in cells.

Tower, an expert on the biology of aging, said that under this hypothesis, aging of the organism is a consequence of natural selection for optimal reproduction. He wondered, though: Is aging is always a negative trait at the level of individual genes?

To test this, Tower and a team of researchers developed a scenario with molecules can replicate themselves. Such molecules are believed to be the evolutionary origin of modern genes.

dna

There are several examples of this biological tradeoff. The gene p53, for example, suppresses cancer, but it is known to accelerate aging in cells. NeuroscienceNews.com image is in the public domain.

Using computer modeling, the researchers paired an unstable short-lived gene, B, and its interactions with a longer-living gene, A, to create a new replicator, AB. In some simulations, the fact that B was short-lived enhanced beneficial aspects of A that would maximize the proliferation of the AB replicator.

“The results suggest that evolution can favor the limited stability of genes as a way to increase complexity and the reproductive fitness of the organism,” Tower said. “Interventions designed to stabilize genes might help combat aging.”

About this neuroscience research article

Funding: The study was funded by grants from the National Institute on Aging.

Source: Emily F Gersema – USC
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Models of Replicator Proliferation Involving Differential Replicator Subunit Stability” by Zewei Li, Runhe Lyu, and John Tower in Origins of Life and Evolution and Biospheres. Published September 10 2018.
doi:10.1007/s11084-018-9561-x

Cite This NeuroscienceNews.com Article
USC”Aging May Be As Old As Life Itself.” NeuroscienceNews. NeuroscienceNews, 12 September 2018.
<http://neurosciencenews.com/genetics-evolution-aging-9854/>.
USC(2018, September 12). Aging May Be As Old As Life Itself. NeuroscienceNews. Retrieved September 12, 2018 from http://neurosciencenews.com/genetics-evolution-aging-9854/
USC”Aging May Be As Old As Life Itself.” http://neurosciencenews.com/genetics-evolution-aging-9854/ (accessed September 12, 2018).

Abstract

Models of Replicator Proliferation Involving Differential Replicator Subunit Stability

Several models for the origin of life involve molecules that are capable of self-replication, such as self-replicating polymers composed of RNA or DNA or amino acids. Here we consider a hypothetical replicator (AB) composed of two subunits, A and B. Programs written in Python and C programming languages were used to model AB replicator abundance as a function of cycles of replication (iterations), under specified hypothetical conditions. Two non-exclusive models describe how a reduced stability for B relative to A can have an advantage for replicator activity and/or evolution by generating free A subunits. In model 1, free A subunits associate with AB replicators to create AAB replicators with greater activity. In simulations, reduced stability of B was beneficial when the replication activity of AAB was greater than two times the replication activity of AB. In model 2, the free A subunit is inactive for some number of iterations before it re-creates the B subunit. A re-creates the B subunit with an equal chance of creating B or B’, where B’ is a mutant that increases AB’ replicator activity relative to AB. In simulations, at moderate number of iterations (< 15), a shorter survival time for B is beneficial when the stability of B is greater than the inactive time of A. The results are consistent with the hypothesis that reduced stability for a replicator subunit can be advantageous under appropriate conditions.[divider]Feel free to share this Neuroscience News.[/divider]

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