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- Chen, Hwei-yen, 1983-, et al.
(författare)
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Condition dependence of male mortality drives the evolution of sex differences in longevity
- 2014
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Ingår i: Current Biology. - : Elsevier BV. - 0960-9822 .- 1879-0445. ; 24:20, s. 2423-2427
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Tidskriftsartikel (refereegranskat)abstract
- Males and females age at different rates and have different life expectancies across the animal kingdom, but what causes the longevity "gender gaps" remains one of the most fiercely debated puzzles among biologists and demographers [1-7]. Classic theory predicts that the sex experiencing higher rate of extrinsic mortality evolves faster aging and reduced longevity [1]. However, condition dependence of mortality [8, 9] can counter this effect by selecting against senescence in whole-organism performance [5, 10]. Contrary to the prevailing view but in line with an emerging new theory [7-9, 11], we show that the evolution of sex difference in longevity depends on the factors that cause sex-specific mortality and cannot be predicted from the mortality rate alone. Experimental evolution in an obligately sexual roundworm, Caenorhabditis remanei, in which males live longer than females, reveals that sexual dimorphism in longevity erodes rapidly when the extrinsic mortality in males is increased at random. We thus experimentally demonstrate evolution of the sexual monomorphism in longevity in a sexually dimorphic organism. Strikingly, when extrinsic mortalityis increased in a way that favors survival of fast-moving individuals, males evolve increased longevities, thereby widening the gender gap. Thus,sex-specific selection on whole-organism performance in males renders them less prone to the ravages of old age than females, despite higher rates of extrinsic mortality. Our results reconcile previous research with recent theoretical breakthroughs [8, 9] by showing that sexual dimorphism inlongevity evolves rapidly and predictably as a result of the sex-specific interactions between environmental hazard and organism's condition.
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| 2. |
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| 3. |
- Chen, Hwei-yen, 1983-
(författare)
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Experimental Evolution of Life-history : Testing the Evolutionary Theories of Ageing
- 2014
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- 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.
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| 4. |
- Chen, Hwei-yen, 1983-, et al.
(författare)
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Germline mutation rate is elevated in young and old parents in Caenorhabditis remanei
- 2023
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Ingår i: Evolution Letters. - : Oxford University Press. - 2056-3744. ; 7:6, s. 478-489
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Tidskriftsartikel (refereegranskat)abstract
- The effect of parental age on germline mutation rate across generations is not fully understood. While some studies report a positive linear relationship of mutation rate with increasing age, others suggest that mutation rate varies with age but not in a linear fashion. We investigated the effect of parental age on germline mutations by generating replicated mutation accumulation lines in Caenorhabditis remanei at three parental ages ("Young T1" [Day 1], "Peak T2" [Day 2], and "Old T5" [Day 5] parents). We conducted whole-genome resequencing and variant calling to compare differences in mutation rates after three generations of mutation accumulation. We found that Peak T2 lines had an overall reduced mutation rate compared to Young T1 and Old T5 lines, but this pattern of the effect varied depending on the variant impact. Specifically, we found no high-impact variants in Peak T2 lines, and modifiers and up- and downstream gene variants were less frequent in these lines. These results suggest that animals at the peak of reproduction have better DNA maintenance and repair compared to young and old animals. We propose that C. remanei start to reproduce before they optimize their DNA maintenance and repair, trading the benefits of earlier onset of reproduction against offspring mutation load. The increase in offspring mutation load with age likely represents germline senescence. Germline mutations play a key role in evolution through the generation of novel genotypes. Estimating the mutation rate in species, populations, and individuals is one way to understand the relative timeframe of evolutionary processes, for the timing of historical events and for estimating heritability of traits and diseases. Individual age at reproduction is known to affect the number of mutations being transferred into the next generation and generally mutation rate is thought to increase with increasing parental age. However, preventing mutations in germ cells is potentially costly and it may pay off to optimize germline genome repair and maintenance during peak reproductive periods, and relax it during nonpeak periods. This idea has been put forward to explain for example the reduction of gonad size in seasonally reproducing animals during nonreproductive periods and supported by the finding that the mutation rate seems to be higher in teenage men compared to men during their peak reproductive ages. We further tested this idea of a nonlinear relationship between age and mutation rate by performing a mutation accumulation experiment in a short-lived nematode. We kept experimental lines and allowed adults to reproduce at different ages in different lines, with some lines reproducing before, some during, and some after their reproductive peak. We found that mutation rates are higher in nematode lines reproducing before or after the reproductive peak compared to those reproducing during the peak. Our results therefore support the idea that germline genome maintenance and repair is potentially costly and that the mutation rate does not just increase with age but is optimized during the peak reproductive age of an organism.
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| 5. |
- Chen, Hwei-yen, 1983-, et al.
(författare)
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Trade-off between somatic and germline repair in a vertebrate supports the expensive germ line hypothesis
- 2020
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences (PNAS). - 0027-8424 .- 1091-6490. ; 117:16, s. 8973-8979
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Tidskriftsartikel (refereegranskat)abstract
- The disposable soma theory is a central tenet of the biology of aging where germline immortality comes at the cost of an aging soma [T. B. L. Kirkwood, Nature 270, 301–304 (1977); T. B. L. Kirkwood, Proc. R. Soc. Lond. B Biol. Sci. 205, 531–546 (1979); T. B. L. Kirkwood, S. N. Austad, Nature 408, 233–238 (2000)]. Limited resources and a possible trade-off between the repair and maintenance of the germ cells and growth and maintenance of the soma may explain the deterioration of the soma over time. Here we show that germline removal allows accelerated somatic healing under stress. We tested “the expensive germ line” hypothesis by generating germline-free zebrafish Danio rerio and testing the effect of the presence and absence of the germ line on somatic repair under benign and stressful conditions. We exposed male fish to sublethal low-dose ionizing radiation, a genotoxic stress affecting the soma and the germ line, and tested how fast the soma recovered following partial fin ablation. We found that somatic recovery from ablation occurred substantially faster in irradiated germline-free fish than in the control germline-carrying fish where somatic recovery was stunned. The germ line did show signs of postirradiation recovery in germline-carrying fish in several traits related to offspring number and fitness. These results support the theoretical conjecture that germline maintenance is costly and directly trades off with somatic maintenance.
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| 6. |
- Lind, Martin I., et al.
(författare)
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Rapamycin additively extends lifespan in short- and long-lived lines of the nematode Caenorhabditis remanei
- 2017
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Ingår i: Experimental Gerontology. - : Elsevier BV. - 0531-5565 .- 1873-6815. ; 90, s. 79-82
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Tidskriftsartikel (refereegranskat)abstract
- Despite tremendous progress in finding genes that, when manipulated, affects lifespan, little is known about the genetics underlying natural variation in lifespan. While segregating genetic variants for lifespan has been notoriously difficult to find in genome-wide association studies (GWAS), a complementary approach is to manipulate key genetic pathways in lines that differ in lifespan. If these candidate pathways are down regulated in long-lived lines, these lines can be predicted to respond less to pharmaceutical down-regulation of these pathways than short-lived lines. Experimental studies have identified the nutrient-sensing pathway TOR as a key regulator of lifespan in model organisms, and this pathway can effectively be down regulated using the drug rapamycin, which extends lifespan in all tested species. We expose short-and long-lived lines of the nematode Caenorhabditis remanei to rapamycin, and investigate if long-lived lines, which are hypothesized to already have down-regulated TOR signaling, respond less to rapamycin. We found no interaction between line and rapamycin treatment, since rapamycin extended lifespan independent of the intrinsic lifespan of the lines. This shows that rapamycin is equally effective on long and short-lived lines, and suggests that the evolution of long life may involve more factors that down-regulation of TOR.
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| 7. |
- Lind, Martin I., et al.
(författare)
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Slow development as an evolutionary cost of long life
- 2017
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Ingår i: Functional Ecology. - : Wiley. - 0269-8463 .- 1365-2435. ; 31:6, s. 1252-1261
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Tidskriftsartikel (refereegranskat)abstract
- Life-history theory predicts a trade-off between early-life fitness and life span. While the focus traditionally has been on the fecundity-life span trade-off, there are strong reasons to expect trade-offs with growth rate and/or development time. We investigated the roles of growth rate and development time in the evolution of life span in two independent selection experiments in the outcrossing nematode Caenorhabditis remanei. First, we found that selection under heat-shock leads to the evolution of increased life span without fecundity costs, but at the cost of slower development. Thereafter, the putative evolutionary links between development time, growth rate, fecundity, heat-shock resistance and life span were independently assessed in the second experiment by directly selecting for fast or slow development. This experiment confirmed our initial findings, since selection for slow development resulted in the evolution of long life span and increased heat-shock resistance. Because there were no consistent trade-offs with growth rate or fecundity, our results highlight the key role of development rate - differentiation of the somatic cells per unit of time - in the evolution of life span. Since development time is under strong selection in nature, reduced somatic maintenance resulting in shorter life span may be a widespread cost of rapid development.
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