It is an inevitability of life – you are born and you begin to age.
Scientists have puzzled over just why organisms evolved aging as a strategy, and now there appears to be an answer. Allowing one individual to carry all the cellular damage inflicted over time, rather than dividing it between two organisms during reproduction, increases the chances that the individual's line will continue to reproduce for many generations to come, a new study indicates.
The earliest organisms, single-celled creatures called prokaryotes, which include bacteria, probably did not age but rather divided damaged material equally among new cells. There was not a parent cell, but rather the original cell divided into two siblings that were, in effect, the same age and shared the damage from the original cell equally.
Somewhere along the way, that strategy changed so that a parent cell retained most of the damage from aging and the offspring started with a mostly clean slate.
"The idea is that the damage has a constant effect on the fitness of the offspring, but if the damage is concentrated in one individual then a lot of damage will be eliminated from the lineage when that individual dies," said Carl Bergstrom, a University of Washington associate professor of biology who participated in the work.
Aging is essentially a decline in reproductive rate and an increase in mortality over time, based on changes in tissues, cells and cellular structures. Those changes can include damage to DNA or damage to cellular material or even organs.
In what is called symmetric reproduction, a cell divides in two and splits the damage equally among the succeeding generation of cells. In asymmetric reproduction, the parent retains the damage associated with aging.
Symmetric reproduction favors a longer life for an individual, but eventually the damage is likely to be so great that a particular line will no longer be able to reproduce. Asymmetric reproduction likely means a shorter life for an individual in exchange for the likely greater longevity of the line.
"If you divide asymmetrically, the survivor is likely to be the undamaged one, which will then be in a better position to produce surviving offspring," Bergstrom said.
The mechanisms that favor asymmetrical aging over symmetry are so general that they are expected to operate in a wide range of organisms, the researchers say. The new work suggests that aging has evolved in most – perhaps even all – types of organisms.
The research is described in a paper in the April edition of the journal Aging Cell. The lead author is Martin Ackermann of the Institute for Integrative Biology in Zurich, Switzerland. Besides Bergstrom, co-authors are Lin Chao of the University of California, San Diego, and Michael Doebeli of the University of British Columbia in Vancouver.
The researchers used mathematical models and computer simulations to examine the likely evolution of aging by distributing damage asymmetrically during reproduction. They also studied the investment an organism makes in a mechanism to repair damage. From their findings, the scientists concluded that reproduction in which damage was distributed asymmetrically would be favored.
The models were altered to allow cells to repair some of their damage, and asymmetric reproduction still was favored. Not only that, but once asymmetric division became the dominant reproduction method the models indicate that evolution will eventually reduce the investment in repair, Bergstrom said.
The implication is that evolution favors individuals aging as a means of allowing their lineage to persist longer.
"A lineage is more likely to survive in the long run if one individual falls on the grenade of its own cellular damage," Bergstrom said.
The work was funded by the Swiss National Science Foundation, the Roche Research Foundation, the Novartis Foundation, the U.S. National Institutes of Health, the James S. McDonnell Foundation and the Natural Sciences and Engineering Research Council of Canada.
For more information, contact Bergstrom at (206) 685-3487 or cbergst@u.washington.edu; or Ackermann at (41) 44 632 69 28 or martin.ackermann@env.ethz.ch
Journal
Aging Cell