Natural selection: Evolution of lifespan in C. elegans

  title={Natural selection: Evolution of lifespan in C. elegans},
  author={David W. Walker and Gawain McColl and Nicole L. Jenkins and Jennifer M. Harris and Gordon J. Lithgow},
It was proposed almost 50 years ago that ageing is non-adaptive and is the consequence of a decline in the force of natural selection with age. This led to the theory that ageing results from detrimental effects late in life of genes that act beneficially in early life, so any genetic alteration that increases lifespan might be expected to reduce fitness, for example. We show here that a mutation that greatly increases the lifespan of the nematode Caenorhabditis elegans does indeed exhibit a… 

Fitness cost of extended lifespan in Caenorhabditis elegans

It is demonstrated by laboratory natural selection that partial loss of function of the insulin receptor–like protein DAF–2 results in dramatically reduced fitness even under laboratory conditions, consistent with an evolutionary theory of aging.

Programmed and altruistic ageing

It is suggested that the similarities between the molecular pathways that regulate ageing in yeast, worms, flies and mice, together with evidence that is consistent with programmed death in salmon and other organisms, raise the possibility that programmed ageing or death can also occur in higher eukaryotes.

Experimental evolution reveals antagonistic pleiotropy in reproductive timing but not life span in Caenorhabditis elegans.

It is concluded that the genetic constraint is not absolute, that is, it is possible to uncouple longevity from early fecundity using genetic variation segregating within and among natural populations.

Antagonistically pleiotropic allele increases lifespan and late-life reproduction at the cost of early-life reproduction and individual fitness

Results suggest that the age-1(hx546) allele has opposing effects on early-life versus late-life fitness in accordance with antagonistic pleiotropy (AP) and disposable soma theories of ageing, and support the theoretical conjecture that experimental studies based on standing genetic variation underestimate the importance of AP.

Stressful environments can indirectly select for increased longevity

It is demonstrated that long-lived, stress-resistant Caenorhabditis elegans age-1(hx546) mutants have higher fitness than the wild-type genotype if mixed genotype populations are periodically exposed to high temperatures when food availability also varies over time.

Cost-free lifespan extension via optimization of gene expression in adulthood aligns with the developmental theory of ageing

Investigation of the consequences for lifespan, reproduction, egg size and individual fitness of early-life, adulthood and post-reproductive onset of RNAi knockdown of five ‘longevity’ genes involved in key biological processes in Caenorhabditis elegans demonstrates that suboptimal gene expression in adulthood often contributes to reduced lifespan directly rather than through competitive resource allocation between reproduction and somatic maintenance.

The ecological genetics of senescence and stress resistance in Caenorhabditis elegans

The results imply that, is genetic variation is present in populations which encounter harsh conditions, increased longevity can evolve as a consequence of selection for greater resistance to stress.

Aging: Evolutionary Theory Meets Genomic Approaches

The evolution of the aging field over the past several years and the implications of the move toward genomics are reviewed, including the scope of cellular processes that influence longevity and the conservation of longevity determinants between organisms are reviewed.

Natural variation in lifespan and stress responses in Caenorhabditis elegans

Analysis of lifespan, dietary restriction, oxidative stress, heat shock and cold shock in a new 4parent panel of 200 sequenced and genotyped recombinant inbred lines (RILs) without the canonical strain N2 shows there is an extensive variation among the RILs under all phenotypic traits.



A C. elegans mutant that lives twice as long as wild type

Finding that mutations in the gene daf-2 can cause fertile, active, adult Caenorhabditis elegans hermaphrodites to live more than twice as long as wild type raises the possibility that the longevity of the dauer is not simply a consequence of its arrested growth, but instead results from a regulated lifespan extension mechanism that can be uncoupled from other aspects of dauer formation.

Movement as an index of vitality: comparing wild type and the age-1 mutant of Caenorhabditis elegans.

  • S. A. DuhonT. Johnson
  • Biology
    The journals of gerontology. Series A, Biological sciences and medical sciences
  • 1995
Cumulative lifetime movements of individuals were highly correlated with, and thus a good predictor of, individual life span, and imply that the physiological process altered by the age-1 mutation results in increased health during later life as monitored by increased ability to move.

Genetic analysis of the roles of daf-28 and age-1 in regulating Caenorhabditis elegans dauer formation.

Daf-28(sa191) acts at a novel point downstream in the genetic pathway for dauer formation and causes a modest increase in life span, which is most similar to those of daf-2 and Daf-23 mutations, which also cause a dramatic increase inLife span.

An insulin-like signaling pathway affects both longevity and reproduction in Caenorhabditis elegans.

Insulin signaling, mediated by DAF-2 through the AGE-1 phosphatidylinositol-3-OH kinase, regulates reproduction and embryonic development, as well as dauer diapause and life span, and that Daf-16 transduces these signals.

Thermotolerance of a long-lived mutant of Caenorhabditis elegans.

It is proposed that the enhanced ability of Age strains to cope with environmental stress may be mechanistically related to their lower age-specific mortality rates.


Natural selection will frequently maximize vigor in youth at the expense of vigor later on and thereby produce a declining vigor (senescence) during adult life, which explains much of what is known of phylogenetic variation in rates of senescence.

Three mutants that extend both mean and maximum life span of the nematode, Caenorhabditis elegans, define the age-1 gene.

Three of four mutant strains studied in the nematode Caenorhabditis elegans contain recessive mutations that significantly lengthen life; MK542 and MK546 consistently fail to complement the long life phenotype of age-1 and are therefore allelic.

A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans

It is suggested that phosphatidylinositol signalling mediated by AGE-1 protein controls lifespan and the dauer diapause decision.

UNSOLVED problem of biology.

  • P. Medawar
  • Medicine, Biology
    The Medical journal of Australia
  • 1953

Thermotolerance and extended life-span conferred by single-gene mutations and induced by thermal stress.

The results suggest that ability to respond to stress limits the life expectancy of C. elegans and might do so in other metazoa as well, and the relationship between increased thermotolerance and increased life-span is investigated.