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Why ageing stops: heterogeneity explains late-life mortality deceleration in nematodes
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Ecology and Genetics, Animal ecology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Ecology and Genetics, Animal ecology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Ecology and Genetics, Animal ecology.
2013 (English)In: Biology Letters, ISSN 1744-9561, E-ISSN 1744-957X, Vol. 9, no 5, 20130217- p.Article in journal (Refereed) Published
Abstract [en]

While ageing is commonly associated with exponential increase in mortality with age, mortality rates paradoxically decelerate late in life resulting in distinct mortality plateaus. Late-life mortality plateaus have been discovered in a broad variety of taxa, including humans, but their origin is hotly debated. One hypothesis argues that deceleration occurs because the individual probability of death stops increasing at very old ages, predicting the evolution of earlier onset of mortality plateaus under increased rate of extrinsic mortality. By contrast, heterogeneity theory suggests that mortality deceleration arises from individual differences in intrinsic lifelong robustness and predicts that variation in robustness between populations will result in differences in mortality deceleration. We used experimental evolution to directly test these predictions by independently manipulating extrinsic mortality rate (high or low) and mortality source (random death or condition-dependent) to create replicate populations of nematodes, Caenorhabditis remanei that differ in the strength of selection in late-life and in the level of lifelong robustness. Late-life mortality deceleration evolved in response to differences in mortality source when mortality rate was held constant, while there was no consistent response to differences in mortality rate. These results provide direct experimental support for the heterogeneity theory of late-life mortality deceleration.

Place, publisher, year, edition, pages
2013. Vol. 9, no 5, 20130217- p.
Keyword [en]
ageing, heterogeneity, mortality plateau, nematodes, robustness, stress
National Category
Natural Sciences
Identifiers
URN: urn:nbn:se:uu:diva-219215DOI: 10.1098/rsbl.2013.0217ISI: 000330289600020OAI: oai:DiVA.org:uu-219215DiVA: diva2:698761
Available from: 2014-02-25 Created: 2014-02-24 Last updated: 2017-12-05Bibliographically approved
In thesis
1. Experimental Evolution of Life-history: Testing the Evolutionary Theories of Ageing
Open this publication in new window or tab >>Experimental Evolution of Life-history: Testing the Evolutionary Theories of Ageing
2014 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Ageing reduces fitness, but how ageing evolves is still unclear. Evolutionary theory of ageing hinges on the fundamental principal that the force of natural selection declines with age. This principle has yielded two important predictions: 1) the evolution of faster ageing in populations under high rate of extrinsic mortality; and 2) the evolution of faster ageing in a sex that experiences higher rates of extrinsic mortality. However, an emerging new theory argues that when the extrinsic mortality is not random but instead selects on traits showing positive genetic correlation with lifespan, increased mortality should lead to the evolution of increased lifespan. Such condition-dependent mortality is also expected to increase the robustness in the population, resulting in increased deceleration of mortality in late-life. Similarly, high sex-specific mortality can result in increased sex-specific selection on traits that have positive pleiotropic effects on lifespan in the affected sex. This thesis is based on two experimental evolution studies in Caenorhabditis remanei. The first experiment was designed to disentangle the effects of the rate (high or low) and the source (random or condition-dependent) of mortality on the evolution of lifespan and ageing. Reduced lifespan evolved under high rate of random mortality, whereas high condition-dependent mortality, imposed by heat-shock, led to the evolution of increased lifespan (Paper I). However, while female reproduction increased under condition-dependent mortality, male reproduction suffered, suggesting a role for sexual antagonism in maintaining genetic variation for fitness (Paper II). Besides, long lifespan and high fecundity evolved at a cost of slow juvenile growth rate in females (Paper III). Moreover, high condition-dependent mortality led to the evolution of lower rate of intrinsic mortality in late-life (Paper IV). The second experiment showed that evolution of sexual dimorphism in lifespan is driven by the factors that cause sex-specific mortality and cannot be predicted from differences in mortality rate alone. Specifically, high condition-dependent mortality renders males less prone to ageing than females despite higher rates of male mortality (Paper V). The strength of this thesis is the reconfirmation of the earlier findings combined with support for the new theory. Rather than further complicating the matter, the inclusion of the new ideas should help explain some empirical results that are inconsistent with the classic theory, as well as provide a more comprehensive picture of ageing evolution.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2014. 43 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Science and Technology, ISSN 1651-6214 ; 1178
Keyword
senescence, ageing, longevity, mortality, experimental evolution, Caenorhabditis remanei
National Category
Natural Sciences
Research subject
Biology
Identifiers
urn:nbn:se:uu:diva-231948 (URN)978-91-554-9034-8 (ISBN)
Public defence
2014-10-28, Friessalen, EBC, Norbyvägen 14, Uppsala, 14:00 (English)
Opponent
Supervisors
Available from: 2014-10-06 Created: 2014-09-11 Last updated: 2015-01-23

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Chen, Hwei-yenMaklakov, Alexei A.

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