scholarly journals Temperature effects on life-history trade-offs, germline maintenance and mutation rate under simulated climate warming

2017 ◽  
Vol 284 (1866) ◽  
pp. 20171721 ◽  
Author(s):  
David Berger ◽  
Josefine Stångberg ◽  
Karl Grieshop ◽  
Ivain Martinossi-Allibert ◽  
Göran Arnqvist

Mutation has a fundamental influence over evolutionary processes, but how evolutionary processes shape mutation rate remains less clear. In asexual unicellular organism, increased mutation rates have been observed in stressful environments and the reigning paradigm ascribes this increase to selection for evolvability. However, this explanation does not apply in sexually reproducing species, where little is known about how the environment affects mutation rate. Here we challenged experimental lines of seed beetle, evolved at ancestral temperature or under simulated climate warming, to repair induced mutations at ancestral and stressful temperature. Results show that temperature stress causes individuals to pass on a greater mutation load to their grand-offspring. This suggests that stress-induced mutation rates, in unicellular and multicellular organisms alike, can result from compromised germline DNA repair in low condition individuals. Moreover, lines adapted to simulated climate warming had evolved increased longevity at the cost of reproduction, and this allocation decision improved germline repair. These results suggest that mutation rates can be modulated by resource allocation trade-offs encompassing life-history traits and the germline and have important implications for rates of adaptation and extinction as well as our understanding of genetic diversity in multicellular organisms.

2013 ◽  
Vol 280 (1750) ◽  
pp. 20122047 ◽  
Author(s):  
Roland R. Regoes ◽  
Steven Hamblin ◽  
Mark M. Tanaka

Many viruses, particularly RNA viruses, mutate at a very high rate per genome per replication. One possible explanation is that high mutation rates are selected to meet the challenge of fluctuating environments, including the host immune response. Alternatively, recent studies argue that viruses evolve under a trade-off between replication speed and fidelity such that fast replication is selected, and, along with it, high mutation rates. Here, in addition to these factors, we consider the role of viral life-history properties: namely, the within-host dynamics of viruses resulting from their interaction with the host. We develop mathematical models incorporating factors occurring within and between hosts, including deleterious and advantageous mutations, host death owing to virulence and clearance of viruses by the host. Beneficial mutations confer both a within-host and a transmission advantage. First, we find that advantageous mutations have only a weak effect on the optimal genomic mutation rate. Second, viral life-history properties have a large effect on the mutation rate. Third, when the speed–fidelity trade-off is included, there can be two locally optimal mutation rates. Our analysis provides a way to consider how life-history properties combine with biochemical trade-offs to shape mutation rates.


1994 ◽  
Vol 346 (1317) ◽  
pp. 333-343 ◽  

High mutation rates are generally considered to be detrimental to the fitness of multicellular organisms because mutations untune finely tuned biological machinery. However, high mutation rates may be favoured by a need to evade an immune system that has been strongly stimulated to recognize those variants that reproduced earlier during the infection, hiv infections conform to this situation because they are characterized by large numbers of viruses that are continually breaking latency and large numbers that are actively replicating throughout a long period of infection. To be transmitted, HIVS are thus generally exposed to an immune system that has been activated to destroy them in response to prior viral replication in the individual. Increases in sexual contact should contribute to this predicament by favouring evolution toward relatively high rates of replication early during infection. Because rapid replication and high mutation rate probably contribute to rapid progression of infections to aids, the interplay of sexual activity, replication rate, and mutation rate helps explain why HIV-1 has only recently caused a lethal pandemic, even though molecular data suggest that it may have been present in humans for more than a century. This interplay also offers an explanation for geographic differences in progression to cancer found among infections due to the other major group of human retroviruses, human T-cell lymphotropic viruses (HTLV). Finally, it suggests ways in which we can use natural selection as a tool to control the aids pandemic and prevent similar pandemics from arising in the future.


1988 ◽  
Vol 66 (8) ◽  
pp. 1906-1912 ◽  
Author(s):  
Todd W. Arnold

Recently, Zammuto (R. M. Zammuto. 1986. Can. J. Zool. 64: 2739–2749) suggested that North American game birds exhibited survival–fecundity trade-offs consistent with the "cost of reproduction" hypothesis. However, there were four serious problems with the data and the analyses that Zammuto used: (i) the species chosen for analysis ("game birds") showed little taxonomic or ecological uniformity, (ii) the measures of future reproductive value (maximum longevity) were severely biased by unequal sample sizes of band recoveries, (iii) the measures of current reproductive effort (clutch sizes) were inappropriate given that most of the birds analyzed produce self-feeding precocial offspring, and (iv) the statistical units used in the majority of analyses (species) were not statistically independent with respect to higher level taxonomy. After correcting these problems, I found little evidence of survival–fecundity trade-offs among precocial game birds, and I attribute most of the explainable variation in life-history traits of these birds to allometry, phylogeny, and geography.


2017 ◽  
Author(s):  
Beth Gibson ◽  
Daniel Wilson ◽  
Edward Feil ◽  
Adam Eyre-Walker

AbstractGeneration time varies widely across organisms and is an important factor in the life cycle, life history and evolution of organisms. Although the doubling time (DT), has been estimated for many bacteria in the lab, it is nearly impossible to directly measure it in the natural environment. However, an estimate can be obtained by measuring the rate at which bacteria accumulate mutations per year in the wild and the rate at which they mutate per generation in the lab. If we assume the mutation rate per generation is the same in the wild and in the lab, and that all mutations in the wild are neutral, an assumption that we show is not very important, then an estimate of the DT can be obtained by dividing the latter by the former. We estimate the DT for four species of bacteria for which we have both an accumulation and a mutation rate estimate. We also infer the distribution of DTs across all bacteria from the distribution of the accumulation and mutation rates. Both analyses suggest that DTs for bacteria in the wild are substantially greater than those in the lab, that they vary by orders of magnitude between different species of bacteria and that a substantial fraction of bacteria double very slowly in the wild.


2018 ◽  
Vol 285 (1880) ◽  
pp. 20180789 ◽  
Author(s):  
Beth Gibson ◽  
Daniel J. Wilson ◽  
Edward Feil ◽  
Adam Eyre-Walker

Generation time varies widely across organisms and is an important factor in the life cycle, life history and evolution of organisms. Although the doubling time (DT) has been estimated for many bacteria in the laboratory, it is nearly impossible to directly measure it in the natural environment. However, an estimate can be obtained by measuring the rate at which bacteria accumulate mutations per year in the wild and the rate at which they mutate per generation in the laboratory. If we assume the mutation rate per generation is the same in the wild and in the laboratory, and that all mutations in the wild are neutral, an assumption that we show is not very important, then an estimate of the DT can be obtained by dividing the latter by the former. We estimate the DT for five species of bacteria for which we have both an accumulation and a mutation rate estimate. We also infer the distribution of DTs across all bacteria from the distribution of the accumulation and mutation rates. Both analyses suggest that DTs for bacteria in the wild are substantially greater than those in the laboratory, that they vary by orders of magnitude between different species of bacteria and that a substantial fraction of bacteria double very slowly in the wild.


Author(s):  
Xin Hao ◽  
Ting‐Ting Zou ◽  
Xing‐Zhi Han ◽  
Fu‐Shun Zhang ◽  
Wei‐Guo Du

Ecology ◽  
1982 ◽  
Vol 63 (3) ◽  
pp. 616-620 ◽  
Author(s):  
Douglas W. Tallamy ◽  
Robert F. Denno

2018 ◽  
Author(s):  
Gregg W.C. Thomas ◽  
Richard J. Wang ◽  
Arthi Puri ◽  
R. Alan Harris ◽  
Muthuswamy Raveendran ◽  
...  

AbstractMutation rates vary between species across several orders of magnitude, with larger organisms having the highest per-generation mutation rates. Hypotheses for this pattern typically invoke physiological or population-genetic constraints imposed on the molecular machinery preventing mutations1. However, continuing germline cell division in multicellular eukaryotes means that organisms with longer generation times and of larger size will leave more mutations to their offspring simply as a by-product of their increased lifespan2,3. Here, we deeply sequence the genomes of 30 owl monkeys (Aotus nancymaae) from 6 multi-generation pedigrees to demonstrate that paternal age is the major factor determining the number of de novo mutations in this species. We find that owl monkeys have an average mutation rate of 0.81 × 10−8 per site per generation, roughly 32% lower than the estimate in humans. Based on a simple model of reproductive longevity that does not require any changes to the mutational machinery, we show that this is the expected mutation rate in owl monkeys. We further demonstrate that our model predicts species-specific mutation rates in other primates, including study-specific mutation rates in humans based on the average paternal age. Our results suggest that variation in life history traits alone can explain variation in the per-generation mutation rate among primates, and perhaps among a wide range of multicellular organisms.


2019 ◽  
Author(s):  
Gretchen F. Wagner ◽  
Emeline Mourocq ◽  
Michael Griesser

Biparental care systems are a valuable model to examine conflict, cooperation, and coordination between unrelated individuals, as the product of the interactions between the parents influences the fitness of both individuals. A common experimental technique for testing coordinated responses to changes in the costs of parental care is to temporarily handicap one parent, inducing a higher cost of providing care. However, dissimilarity in experimental designs of these studies has hindered interspecific comparisons of the patterns of cost distribution between parents and offspring. Here we apply a comparative experimental approach by handicapping a parent at nests of five bird species using the same experimental treatment. In some species, a decrease in care by a handicapped parent was compensated by its partner, while in others the increased costs of care were shunted to the offspring. Parental responses to an increased cost of care primarily depended on the total duration of care that offspring require. However, life history pace (i.e., adult survival and fecundity) did not influence parental decisions when faced with a higher cost of caring. Our study highlights that a greater attention to intergenerational trade-offs is warranted, particularly in species with a large burden of parental care. Moreover, we demonstrate that parental care decisions may be weighed more against physiological workload constraints than against future prospects of reproduction, supporting evidence that avian species may devote comparable amounts of energy into survival, regardless of life history strategy.


2017 ◽  
Vol 49 (6) ◽  
pp. 783 ◽  
Author(s):  
Yan WANG ◽  
Zhenchao LIN ◽  
Bowen HOU ◽  
Shijin SUN

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