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Aging as the Evolutionary Cost of Complexity, Driven by Mitochondrial Dynamics

This popular science article walks through a new interpretation of one class of evolutionary theory of aging, envisaging the existence of aging as being necessary for the formation of complex life forms with active metabolism and high energy demands. While there are higher species that exhibit negligible senescence for much of their lifespans, such as naked mole rats and lobsters, the only definitively immortal animals are lower species such as hydra, and even then only in optimal conditions. It isn't necessary for aging to be essential for it to dominate, however: it would only need to be significantly advantageous in evolutionary competition to reach the situation we see today, in which aging is near ubiquitous in the animal world. This is nonetheless an interesting take on the current body of theory regarding the origins of aging, and dovetails nicely with the significance of mitochondria to aging today:

Life's ever-repeating cycles of birth and death are among the most fundamental principles of nature. An organism starts out as a single cell that grows and divides, develops into an embryo, matures and reaches adulthood, but then ages, deteriorates, and eventually succumbs to death. But why does life have to be cyclic, and why does it have to end in senescence and death? After all, animals like corals and marine sponges live for thousands of years and are capable of virtually infinite regeneration and cell repair. Even in more complex animals, offspring do not inherit their parents' age: every new generation starts with cells in a pristine state, with no trace of aging. If senescence is somehow suppressed in reproductive cells, why do the rest of the organism's tissues end up deteriorating and dying?

At the end of the 19th century, the German biologist August Weismann realized that complex organisms consist of two cell types: the "immortal" germline - eternally young cells that give rise to sperm and eggs - and the "disposable" somatic cells that form the rest of the body. More recently, Weismann's ideas were given an overhaul by Thomas Kirkwood in his disposability theory of aging. Kirkwood argued that the force of natural selection declines with age, as most organisms in their natural environments die due to external hazards such as predators, parasites and starvation. At the same time, organisms must invest resources into both the reproductive effort and the maintenance and repair of their somatic cells. But because the probability of surviving external threats declines with time, the optimal strategy is to allocate less and less resources into somatic maintenance as time goes by. Lack of cell repair in the later stages of the life cycle results in the progressive loss of function and gradual decay - aging.

The real-world picture turned out to be more complex than Weismann's model could have predicted. In complex animals like mammals, birds and insects, Weismann's assumption of the rigid germline-somatic cell distinction holds true: only a relatively small group of cells in an adult retain reproductive potential, while the rest become irreversibly differentiated into somatic tissue cells - liver, skin, muscle - that cannot give rise to a new organism. But this is not the case in the most ancient members of the kingdom, such as hydrae, corals and sponges. Even in their adult forms, these organisms maintain large populations of universal stem cells that can generate both somatic and reproductive cells, that is, germline and somatic cells never really segregate. It is the lack of germline sequestration that gives corals and their relatives the power of regeneration and vegetative plant-like reproduction.

Rather than being universal to all animals, the Weismann barrier appears to be a relatively recent innovation of complex organisms, evolving together with somatic aging and death. What drove the evolution of this separation is not clear, but the answer will also shed light on the origin of mortality in complex animals. There are signs that the evolution of both the germline and mortal somatic cells is related to cellular energetics. Animal cells produce energy through respiration in their mitochondria - the organelles of bacterial origin that retain their own tiny genomes, distinct from the chromosomes housed within the nucleus. Each cell contains tens and hundreds of mitochondria, and each mitochondrion has several DNA molecules. This tiny genome regulates mitochondrial function; its integrity is crucial to cellular respiration, as defective mitochondrial genes often lead to debilitating diseases, neuromuscular degeneration and early death. A large part of mitochondrial gene defects arise from random copying errors in imprecise DNA replication.

Since a large part of mitochondrial gene defects arise from random copying errors in imprecise DNA replication, as cells in a developing organism divide, their mitochondria replicate too, each time introducing new DNA mutations. In our recent scientific paper, we show that in organisms with fast mitochondrial defect accumulation, natural selection favors segregation of an isolated germline with a lower number of cell replication cycles, as it minimizes the damage to the energy-producing organelles that could potentially be transmitted to the next generation. If the pace of error accumulation is slow, however, the strict germline-somatic cell barrier should not evolve. Our model therefore suggests that "disposable" somatic cells, that gave rise to aging and mortality, has evolved as a strategy to maintain mitochondrial quality in complex organisms with multiple tissues and high energy requirements, in which mitochondrial defects accumulate relatively fast.

Link: https://singularityhub.com/2017/01/15/aging-and-death-are-the-evolutionary-price-of-complexity/

Comments

Very interesting--I wonder how this relates to Williams' theory of antagonistic pleiotropy, which I always took to be a relatively good bet on the evolutionary emergence of aging. Williams' view (so far as I understand it) is that of aging is a result of mechanisms that are adaptations in multicellular organisms to the threat of cancer, and those mechanisms have long-term negative consequences (but that's fine from the standpoint of evolution as long as the negative consequences come after the reproductive phase of the organism). Would the view in the article be supplemental to Williams' view, vice versa, or an alternate account?

Posted by: gheme at January 18th, 2017 3:48 PM

I find the phase disposal soma very distracting, I would suggest a more modern term. I do not disagree with this, but unless they can put forth a hypothesis whereby this evolutionary theroy is useful in mitigating aging, I do not see that it has much value. It is still just aging based upon accumulated damage.

Posted by: JohnD at January 18th, 2017 7:36 PM

I haven't read much evolutionary theory. But as a lay person, this theory appeals to me. First, this whole free radical business reminds me of the combustion engine, inefficient due to the heat that it creates. We have improved the combustion engine. We ought to be able to engineer better batteries in our cells, that is, more efficient mitochrondria. I know, the preferred anti aging approach is clearing accumulated damage. But this theory gives me hope on the metabolic pathway front. As a lay person, I see no reason why the efficiency can't be engineered to do more then CR in theory. On the other hand, the cancer threat theory makes tinkering with metabolic pathways seem ominous to me, as the cancer threat could always be lurking.

Posted by: NY2LA at January 18th, 2017 11:23 PM

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