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Longer life span evolves under high rates of condition-dependent mortality
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.
2012 (English)In: Current Biology, ISSN 0960-9822, E-ISSN 1879-0445, Vol. 22, no 22, 2140-2143 p.Article in journal (Refereed) Published
Abstract [en]

Aging affects nearly all organisms, but how aging evolves is still unclear [1-5]. The central prediction of classic theory is that high extrinsic mortality leads to accelerated aging and shorter intrinsic life span [6, 7]. However, this prediction considers mortality as a random process, whereas mortality in nature is likely to be condition dependent. Therefore, the novel theory maintains that condition dependence may dramatically alter, and even reverse, the classic pattern [2-4]. We present experimental evidence for the evolution of longer life span under high condition-dependent mortality. We employed an experimental evolution design, using a nematode, Caenorhabditis remanei, that allowed us to disentangle the effects of mortality rate (high versus low) and mortality source (random versus condition dependent). We observed the evolution of shorter life span under high random mortality, confirming the classic prediction. In contrast, high condition-dependent mortality led to the evolution of longer life span, supporting a key role of condition dependence in the evolution of aging. This life-span extension was not the result of a trade-off with reproduction. By simultaneously corroborating the classic results [8-10] and providing the first experimental evidence for the novel theory [2-4], our study resolves apparent contradictions in the study of aging and challenges the traditional paradigm by demonstrating that condition-environment interactions dictate the evolutionary trajectory of aging.

Place, publisher, year, edition, pages
2012. Vol. 22, no 22, 2140-2143 p.
National Category
Natural Sciences
Identifiers
URN: urn:nbn:se:uu:diva-188135DOI: 10.1016/j.cub.2012.09.021ISI: 000311523800022OAI: oai:DiVA.org:uu-188135DiVA: diva2:576315
Available from: 2012-12-12 Created: 2012-12-12 Last updated: 2017-12-07Bibliographically 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

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