Species Age limit tied to 3200 lifetime genetic mutations

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Discussion Overview

The discussion revolves around the correlation between lifetime genetic mutations and lifespan across various species, particularly focusing on a claim that approximately 3200 mutations accumulate over an individual's lifespan. Participants explore the implications of this correlation, its evolutionary significance, and related biological concepts.

Discussion Character

  • Debate/contested
  • Conceptual clarification
  • Technical explanation

Main Points Raised

  • Some participants note that the reported study primarily involves mammals, suggesting that the findings may not be applicable to a broader range of species, including plants and fungi.
  • One participant references a known correlation between resting heart rate and lifespan in mammals, indicating that there are multiple factors influencing longevity.
  • Another participant discusses how mutation rates can be influenced by evolutionary processes, including DNA replication fidelity and error correction mechanisms, and how these rates may affect adaptability.
  • Some participants express skepticism about the relationship between lifespan and genetic mutations, arguing that only mutations occurring during an organism's fertile period are relevant for evolutionary success.
  • One viewpoint suggests that mutations may simply reflect the number of cell divisions rather than indicating a causal relationship with aging, citing the Hayflick limit as a factor in cellular aging.
  • There is mention of the "Rate of Living" theory, which posits a connection between metabolic rate and lifespan, particularly in mammals.

Areas of Agreement / Disagreement

Participants do not reach a consensus on the relationship between genetic mutations and lifespan. There are competing views regarding the significance of mutations, the relevance of the study's scope, and the underlying biological mechanisms at play.

Contextual Notes

Limitations include the focus on mammals in the study, potential missing assumptions regarding the applicability of findings to other species, and unresolved discussions about the mechanisms of mutation rates and their evolutionary implications.

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TL;DR
Nature magazine article reports tie between lifetime mutations and life span across a wide variety of species.
It is reported that todays issue of Nature Magazine includes an article reporting a correlation between typical total life time gene mutations and typical life span in a variety of species. I do not subscribe to that magazine and have not it or its abstract on the web.

But ... in an article in Science Daily that reports on that article, it is claimed that a group from Wellcome Trust Sanger Institute has found that the number of mutations accumulated by a species over an individuals typical life span is about 3200 - and that this value can be applied across a wide range of species.

My interpretation is that as a species evolves, genetic age-lengthening strategies tend to pay off until about 3200 mutations have formed. At which point extending life become a Darwinian "loosing cause".
 
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This is a study of only mammals (things with hair) not a wide range of animal species, and not plants or fungi.
There are other correlations that go with age.
A well known one is the https://www.researchgate.net/publication/23486438_Heart_rate_lifespan_and_mortality_risk in mammals:
An increasing body of scientific research and observational evidence indicates that resting heart rate (HR) is inversely related to the lifespan among homeothermic mammals and within individual species.

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Mutation rates are can be controlled to some degree by evolutionary processes through fidelity of replications and error correcting mechanisms.

Abstract​


Evolutionary success of bacteria relies on the constant fine-tuning of their mutation rates, which optimizes their adaptability to constantly changing environmental conditions. When adaptation is limited by the mutation supply rate, under some conditions, natural selection favours increased mutation rates by acting on allelic variation of the genetic systems that control fidelity of DNA replication and repair. Mutator alleles are carried to high frequency through hitchhiking with the adaptive mutations they generate. However, when fitness gain no longer counterbalances the fitness loss due to continuous generation of deleterious mutations, natural selection favours reduction of mutation rates. Selection and counter-selection of high mutation rates depends on many factors: the number of mutations required for adaptation, the strength of mutator alleles, bacterial population size, competition with other strains, migration, and spatial and temporal environmental heterogeneity. Such modulations of mutation rates may also play a role in the evolution of antibiotic resistance.
 
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Everything looks good on a log plot.
 
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Also on a log. Less so on a plot.
 
I don't think the idea of lifespan being related to genetic mutations makes much sense, from an evolutionary point of view its only the mutations present during an animal's fertile period that can transmitted. When an animal is no longer fertile, the mechanisms responsible for DNA repair quickly degrade. This is one of the reasons that its difficult to make much sense of human longevity, which is exceptional, as resulting through natural selection. Though even in humans, women who have several health advantages over men, quickly lose them in the period following the menopause, nature apparently has little interest when reproduction stops.
It would seem a little strange to consider genetic mutations as anything more than a reflection of an average age, mutations occur during cell division so most occur during foetal development and early life, while some of these may be transmitted, selection for longevity would require the genes to be able to predict the organism's future. In the wild few animals ever reach their potential lifespan, the chances are that the mutations simply reflect the number of cell divisions over time, it doesn't add anything to suggest a causal relationship with ageing. The relationship between age and death is already well established.
One popular idea is based on the idea that cells have a finite number of divisions before programmed cell death occurs, this is the Hayflick limit, which in humans is estimated to be between 40 - 60 divisions. This would set the maximum possible age for humans to be around 120. It's suggested that this is controlled by telomere length.
There also seems to be a relationship between metabolic rate (including temperature and heart rate) and lifespan, particularly in mammals, this is usually called the "Rate of Living" theory, the higher the rate the shorter the lifespan.
 
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