scholarly journals Plastic responses to novel environments are biased towards phenotype dimensions with high additive genetic variation

2019 ◽  
Vol 116 (27) ◽  
pp. 13452-13461 ◽  
Author(s):  
Daniel W. A. Noble ◽  
Reinder Radersma ◽  
Tobias Uller

Environmentally induced phenotypes have been proposed to initiate and bias adaptive evolutionary change toward particular directions. The potential for this to happen depends in part on how well plastic responses are aligned with the additive genetic variance and covariance in traits. Using meta-analysis, we demonstrate that plastic responses to novel environments tend to occur along phenotype dimensions that harbor substantial amounts of additive genetic variation. This suggests that selection for or against environmentally induced phenotypes typically will be effective. One interpretation of the alignment between the direction of plasticity and the main axis of additive genetic variation is that developmental systems tend to respond to environmental novelty as they do to genetic mutation. This makes it challenging to distinguish if the direction of evolution is biased by plasticity or genetic “constraint.” Our results therefore highlight a need for new theoretical and empirical approaches to address the role of plasticity in evolution.

2020 ◽  
Author(s):  
Franziska S. Brunner ◽  
Alan Reynolds ◽  
Ian W. Wilson ◽  
Stephen Price ◽  
Steve Paterson ◽  
...  

ABSTRACTGenotype-by-environment interactions (G x E) underpin the evolution of plastic responses in natural populations. Theory assumes that G x E interactions exist but empirical evidence from natural populations is equivocal and difficult to interpret because G x E interactions are normally univariate plastic responses to a single environmental gradient. We compared multivariate plastic responses of 43 Daphnia magna clones from the same population in a factorial experiment that crossed temperature and food environments. Multivariate plastic responses explained more than 30% of the total phenotypic variation in each environment. G x E interactions were detected in most environment combinations irrespective of the methodology used. However, the nature of G x E interactions was context-dependent and led to environment-specific differences in additive genetic variation (G-matrices). Clones that deviated from the population average plastic response were not the same in each environmental context and there was no difference in whether clones varied in the nature (phenotypic integration) or magnitude of their plastic response in different environments. Plastic responses to food were aligned with additive genetic variation (gmax) at both temperatures, whereas plastic responses to temperature were not aligned with additive genetic variation (gmax) in either food environment. These results suggest that fundamental differences may exist in the potential for our population to evolve novel responses to food versus temperature changes, and challenges past interpretations of thermal adaptation based on univariate studies.


2000 ◽  
Vol 71 (3) ◽  
pp. 713-724 ◽  
Author(s):  
Maire Rantala ◽  
Tapio T Rantala ◽  
Markku J Savolainen ◽  
Yechiel Friedlander ◽  
Y Antero Kesäniemi

2001 ◽  
Vol 73 (3) ◽  
pp. 375-387 ◽  
Author(s):  
M. Henryon ◽  
P. Berg ◽  
J. Jensen ◽  
S. Andersen

AbstractThe objective of this study was to test that genetic variation for resistance to clinical and subclinical diseases exists in growing pigs. A total of 13 551 male growing pigs were assessed for resistance to five categories of clinical and subclinical disease: (i) any clinical or subclinical disease, (ii) lameness, (iii) respiratory diseases, (iv) diarrhoea, and (v) other diseases (i.e. any clinical or subclinical disease with the exception of (ii), (iii), and (iv)). Additive genetic variation for resistance to each disease category was estimated by fitting a Weibull, sire-dam frailty model to time until the pigs were first diagnosed with a disease from that category. Genetic correlations among the resistances to each disease category were approximated as product-moment correlations among predicted breeding values of the sires. Additive genetic variation was detected for resistance to (i) any clinical or subclinical disease (additive genetic variance for log-frailty (± s.e.) = 0·18 ± 0·05, heritability on the logarithmic-time scale = 0·10), (ii) lameness (0·29 ± 0·11, 0·16), (iii) respiratory diseases (0·24 ± 0·16, 0·12), (iv) diarrhoea (0·30 ± 0·27, 0·16), and (v) the other diseases (0·34 ± 0·15, 0·19) and there were generally positive and low-to-moderate correlations among the predicted breeding values (-0·03 to + 0·65). These results demonstrate that additive genetic variation for resistance to clinical and subclinical diseases does exist in growing pigs, and suggests that selective breeding for resistance could be successful.


2020 ◽  
Author(s):  
Greg M. Walter ◽  
James Clark ◽  
Delia Terranova ◽  
Salvatore Cozzolino ◽  
Antonia Cristaudo ◽  
...  

AbstractAdaptive plasticity increases population persistence, but can slow adaptation to changing environments by hiding the effects of different alleles on fitness. However, if plastic responses are no longer adaptive in novel environments, then differences among alleles can emerge and increase genetic variation in fitness that allows rapid adaptation. We tested this hypothesis by transplanting cuttings and seeds of a Sicilian daisy within and outside its native range, and quantifying variation in morphology, physiology, gene expression and fitness. We show that genetic variance in plasticity increases the potential for rapid adaptation to novel environments. Genetic variation in fitness was low across native environments where plasticity effectively tracked familiar environments. In the novel environment however, genetic variation in fitness increased threefold, and correlated with genetic variation in plasticity. Furthermore, genetic variation that can increase fitness in the novel environment had the lowest fitness at the native site, suggesting that adaptation to novel environments relies on genetic variation in plasticity that is selected against in native environments.


PLoS Genetics ◽  
2014 ◽  
Vol 10 (12) ◽  
pp. e1004854 ◽  
Author(s):  
Anke Tönjes ◽  
Markus Scholz ◽  
Jana Breitfeld ◽  
Carola Marzi ◽  
Harald Grallert ◽  
...  

2018 ◽  
Vol 39 (3) ◽  
pp. 427-439 ◽  
Author(s):  
José A Ramírez-Valiente ◽  
Julie R Etterson ◽  
Nicholas J Deacon ◽  
Jeannine Cavender-Bares

Abstract Heritable variation in polygenic (quantitative) traits is critical for adaptive evolution and is especially important in this era of rapid climate change. In this study, we examined the levels of quantitative genetic variation of populations of the tropical tree Quercus oleoides Cham. and Schlect. for a suite of traits related to resource use and drought resistance. We tested whether quantitative genetic variation differed across traits, populations and watering treatments. We also tested potential evolutionary factors that might have shaped such a pattern: selection by climate and genetic drift. We measured 15 functional traits on 1322 1-year-old seedlings of 84 maternal half-sib families originating from five populations growing under two watering treatments in a greenhouse. We estimated the additive genetic variance, coefficient of additive genetic variation and narrow-sense heritability for each combination of traits, populations and treatments. In addition, we genotyped a total of 119 individuals (with at least 20 individuals per population) using nuclear microsatellites to estimate genetic diversity and population genetic structure. Our results showed that gas exchange traits and growth exhibited strikingly high quantitative genetic variation compared with traits related to leaf morphology, anatomy and photochemistry. Quantitative genetic variation differed between populations even at geographical scales as small as a few kilometers. Climate was associated with quantitative genetic variation, but only weakly. Genetic structure and diversity in neutral markers did not relate to coefficient of additive genetic variation. Our study demonstrates that quantitative genetic variation is not homogeneous across traits and populations of Q. oleoides. More importantly, our findings suggest that predictions about potential responses of species to climate change need to consider population-specific evolutionary characteristics.


2020 ◽  
Author(s):  
Kristi Krebs ◽  
Jonas Bovijn ◽  
Maarja Lepamets ◽  
Jenny C Censin ◽  
Tuuli Jürgenson ◽  
...  

AbstractBackgroundHypersensitivity reactions to drugs are often unpredictable and can be life-threatening, underscoring a need for understanding their underlying mechanisms and risk factors. The extent to which germline genetic variation influences the risk of commonly reported drug allergies such as penicillin allergy remains largely unknown.MethodsWe extracted data from the electronic health records of 52,000 Estonian and 500,000 UK biobank participants to study the role of genetic variation in the occurrence of penicillin hypersensitivity reactions. We used imputed SNP to HLA typing data from up to 22,554 and 488,377 individuals from the Estonian and UK cohorts, respectively, to further fine-map the human leukocyte antigen (HLA) association and replicated our results in two additional cohorts involving a total of 1.14 million individuals.ResultsGenome-wide meta-analysis of penicillin allergy revealed a significant association located in the HLA region on chromosome 6. The signal was further fine-mapped to the HLA-B*55:01 allele (OR 1.47 95% CI 1.37-1.58, P-value 4.63×10-26) and confirmed by independent replication in two cohorts. The meta-analysis of all four cohorts in the study revealed a strong association of HLA-B*55:01 allele with penicillin allergy (OR 1.33 95% CI 1.29-1.37, P-value 2.23×10-72). In silico follow-up suggests a potential effect on T lymphocytes at HLA-B*55:01.ConclusionWe present the first robust evidence for the role of an allele of the major histocompatibility complex (MHC) I gene HLA-B in the occurrence of penicillin allergy.


2013 ◽  
Vol 18 (1) ◽  
pp. 1-18 ◽  
Author(s):  
Robert J. Barth

Abstract Scientific findings have indicated that psychological and social factors are the driving forces behind most chronic benign pain presentations, especially in a claim context, and are relevant to at least three of the AMA Guides publications: AMA Guides to Evaluation of Disease and Injury Causation, AMA Guides to Work Ability and Return to Work, and AMA Guides to the Evaluation of Permanent Impairment. The author reviews and summarizes studies that have identified the dominant role of financial, psychological, and other non–general medicine factors in patients who report low back pain. For example, one meta-analysis found that compensation results in an increase in pain perception and a reduction in the ability to benefit from medical and psychological treatment. Other studies have found a correlation between the level of compensation and health outcomes (greater compensation is associated with worse outcomes), and legal systems that discourage compensation for pain produce better health outcomes. One study found that, among persons with carpal tunnel syndrome, claimants had worse outcomes than nonclaimants despite receiving more treatment; another examined the problematic relationship between complex regional pain syndrome (CRPS) and compensation and found that cases of CRPS are dominated by legal claims, a disparity that highlights the dominant role of compensation. Workers’ compensation claimants are almost never evaluated for personality disorders or mental illness. The article concludes with recommendations that evaluators can consider in individual cases.


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