scholarly journals The genetics of morphological and behavioural island traits in deer mice

2019 ◽  
Vol 286 (1914) ◽  
pp. 20191697 ◽  
Author(s):  
Felix Baier ◽  
Hopi E. Hoekstra

Animals on islands often exhibit dramatic differences in morphology and behaviour compared with mainland individuals, a phenomenon known as the ‘island syndrome’. These differences are thought to be adaptations to island environments, but the extent to which they have a genetic basis or instead represent plastic responses to environmental extremes is often unknown. Here, we revisit a classic case of island syndrome in deer mice ( Peromyscus maniculatus ) from British Columbia. We first show that Saturna Island mice and those from neighbouring islands are approximately 35% (approx. 5 g) heavier than mainland mice and diverged approximately 10 000 years ago. We then establish laboratory colonies and find that Saturna Island mice are heavier both because they are longer and have disproportionately more lean mass. These trait differences are maintained in second-generation captive-born mice raised in a common environment. In addition, island–mainland hybrids reveal a maternal genetic effect on body weight. Using behavioural testing in the laboratory, we also find that wild-caught island mice are less aggressive than mainland mice; however, laboratory-raised mice born to these founders do not differ in aggression. Together, our results reveal that these mice have different responses to the environmental conditions on islands—a heritable change in a morphological trait and a plastic response in a behavioural trait.

2018 ◽  
Author(s):  
Felix Baier ◽  
Hopi E. Hoekstra

ABSTRACTAnimals on islands often exhibit dramatic differences in morphology and behaviour compared to mainland individuals, a phenomenon known as the “island syndrome”. These differences are thought to be adaptations to island environments, but the extent to which they have a genetic basis or instead represent plastic responses to environmental extremes is often unknown. Here, we revisit a classic case of island syndrome in deer mice (Peromyscus maniculatus) from British Columbia. We first show that Saturna Island mice and those from neighbouring islands are ∼35% (∼5g) heavier than mainland mice and diverged approximately 10 thousand years ago. We then established laboratory colonies and find that Saturna Island mice are heavier both because they are longer and have disproportionately more lean mass. These trait differences are maintained in second-generation captive-born mice raised in a common environment. In addition, island-mainland hybrids reveal a maternal genetic effect on body weight. Using behavioural testing in the lab, we also find that wild-caught island mice are less aggressive than mainland mice; however, lab-raised mice born to these founders do not differ in aggression. Together, our results reveal that these mice respond differently to environmental conditions on islands – evolving both heritable changes in a morphological trait and also expressing a plastic phenotypic response in a behavioural trait.


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.


1992 ◽  
Vol 263 (4) ◽  
pp. R820-R826 ◽  
Author(s):  
J. L. Blank ◽  
T. Ruf

Thermoregulatory responses were evaluated in male deer mice (Peromyscus maniculatus nebrascensis) after exposure to short photoperiod and either warm or cold ambient temperature (T(a)). Deer mice were chosen for this study because males exhibit differential reproductive responses to short day length (SD); this difference has a genetic basis, and both phenotypes are found within natural breeding populations. Deer mice undergoing SD-induced gonadal regression significantly improved their cold limit to -32.9 degrees C after exposure to SD/warm T(a) and to -47.4 degrees C after SD/cold T(a) exposure, relative to long day length/warm T(a) controls (-17.4 degrees C). In contrast, deer mice maintaining reproductive function despite SD exposure significantly improved cold limit to -27.2 degrees C only after exposure to SD/cold T(a), relative to controls (-16.3 degrees C). Maximum norepinephrine-induced nonshivering thermogenesis (NST) did not vary with reproductive state, indicating differences in cold tolerance were not due to capacity to produce heat by NST. Comparison between phenotypes of heat production during cold tolerance tests indicated that greater cold tolerance among mice exhibiting SD-induced gonadal regression can be accounted for by 1) lower rates of heat loss and 2) greater improvement of heat production. These findings suggest a functional relationship between reproductive function and seasonal thermoregulatory adjustments and indicate a significant cost to breeding during the winter months.


2019 ◽  
Vol 2019 (1) ◽  
pp. 190-198
Author(s):  
Philip L G Birget ◽  
Petra Schneider ◽  
Aidan J O’Donnell ◽  
Sarah E Reece

Abstract Background and objectives Phenotypic plasticity enables organisms to maximize fitness by matching trait values to different environments. Such adaptive phenotypic plasticity is exhibited by parasites, which experience frequent environmental changes during their life cycle, between individual hosts and also in within-host conditions experienced during infections. Life history theory predicts that the evolution of adaptive phenotypic plasticity is limited by costs and constraints, but tests of these concepts are scarce. Methodology Here, we induce phenotypic plasticity in malaria parasites to test whether mounting a plastic response to an environmental perturbation constrains subsequent plastic responses to further environmental change. Specifically, we perturb red blood cell resource availability to induce Plasmodium chabaudi to alter the trait values of several phenotypes underpinning within-host replication and between-host transmission. We then transfer parasites to unperturbed hosts to examine whether constraints govern the parasites’ ability to alter these phenotypes in response to their new in-host environment. Results Parasites alter trait values in response to the within-host environment they are exposed to. We do not detect negative consequences, for within-host replication or between-host transmission, of previously mounting a plastic response to a perturbed within-host environment. Conclusions and implications We suggest that malaria parasites are highly plastic and adapted to adjusting their phenotypes in response to the frequent changes in the within-host conditions they experience during infections. Our findings support the growing body of evidence that medical interventions, such as anti-parasite drugs, induce plastic responses that are adaptive and can facilitate the survival and potentially, drug resistance of parasites. Lay Summary Malaria parasites have evolved flexible strategies to cope with the changing conditions they experience during infections. We show that using such flexible strategies does not impact upon the parasites’ ability to grow (resulting in disease symptoms) or transmit (spreading the disease).


2006 ◽  
Vol 37 (2) ◽  
pp. 163-180 ◽  
Author(s):  
JONATHAN FLINT ◽  
MARCUS R. MUNAFÒ

The idea that some phenotypes bear a closer relationship to the biological processes that give rise to psychiatric illness than diagnostic categories has attracted considerable interest. Much effort has been devoted to finding such endophenotypes, partly because it is believed that the genetic basis of endophenotypes will be easier to analyse than that of psychiatric disease. This belief depends in part on the assumption that the effect sizes of genetic loci contributing to endophenotypes are larger than those contributing to disease susceptibility, hence increasing the chance that genetic linkage and association tests will detect them. We examine this assumption by applying meta-analytical techniques to genetic association studies of endophenotypes. We find that the genetic effect sizes of the loci examined to date are no larger than those reported for other phenotypes. A review of the genetic architecture of traits in model organisms also provides no support for the view that the effect sizes of loci contributing to phenotypes closer to the biological basis of disease is any larger than those contributing to disease itself. While endophenotype measures may afford greater reliability, it should not be assumed that they will also demonstrate simpler genetic architecture.


2017 ◽  
Author(s):  
Thomas D. Brekke ◽  
Katherine A. Steele ◽  
John F. Mulley

ABSTRACTNon-model rodents are widely used as subjects for both basic and applied biological research, but the genetic diversity of the study individuals is rarely quantified. University-housed colonies tend to be small and subject to founder effects and genetic drift and so may be highly inbred or show substantial genetic divergence from other colonies, even those derived from the same source. Disregard for the levels of genetic diversity in an animal colony may result in a failure to replicate results if a different colony is used to repeat an experiment, as different colonies may have fixed alternative variants. Here we use high throughput sequencing to demonstrate genetic divergence in three isolated colonies of Mongolian gerbil (Meriones unguiculatus) even though they were all established recently from the same source. We also show that genetic diversity in allegedly ‘outbred’ colonies of non-model rodents (gerbils, hamsters, house mice, and deer mice) varies considerably from nearly no segregating diversity, to very high levels of polymorphism. We conclude that genetic divergence in isolated colonies may play an important role in the ‘replication crisis’. In a more positive light, divergent rodent colonies represent an opportunity to leverage genetically distinct individuals in genetic crossing experiments. In sum, awareness of the genetic diversity of an animal colony is paramount as it allows researchers to properly replicate experiments and also to capitalize on other, genetically distinct individuals to explore the genetic basis of a trait.


2001 ◽  
Vol 179 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Alastair G. Cardno ◽  
Pak C. Sham ◽  
Robin M. Murray ◽  
Peter McGuffin

BackgroundSymptomatology in psychoses can be summarised as quantitative symptom dimensions, but their genetic basis is unknown.AimsTo investigate whether genes make an important contribution to symptom dimensions.MethodA total of 224 probandwise twin pairs (106 monozygotic, 118 same-gender dizygotic) where probands had psychosis were ascertained from the Maudsley Twin Register in London. Factor analysis was performed on lifetime symptoms rated on the Operational Checklist for Psychotic Disorders (OPCRIT). Correlations of dimension scores within monozygotic and dizygotic pairs concordant for Research Diagnostic Criteria psychoses were performed. Relationships between dimension scores and genetic loading for psychoses were assessed using logistic regression.ResultsPatterns of familial aggregation consistent with a genetic effect were found for the disorganised dimension and for some measures of the negative, manic and general psychotic dimensions. Disorganised dimension scores were related significantly to genetic loading for psychoses.ConclusionsThe disorganised dimension, and possibly other symptom dimensions, may be useful phenotypes for molecular genetic studies of psychoses.


2016 ◽  
Vol 6 (12) ◽  
pp. 4009-4022 ◽  
Author(s):  
Ilkka Kronholm ◽  
Hanna Johannesson ◽  
Tarmo Ketola

Abstract Phenotypic plasticity is the ability of a genotype to produce different phenotypes under different environmental or developmental conditions. Phenotypic plasticity is a ubiquitous feature of living organisms, and is typically based on variable patterns of gene expression. However, the mechanisms by which gene expression is influenced and regulated during plastic responses are poorly understood in most organisms. While modifications to DNA and histone proteins have been implicated as likely candidates for generating and regulating phenotypic plasticity, specific details of each modification and its mode of operation have remained largely unknown. In this study, we investigated how epigenetic mechanisms affect phenotypic plasticity in the filamentous fungus Neurospora crassa. By measuring reaction norms of strains that are deficient in one of several key physiological processes, we show that epigenetic mechanisms play a role in homeostasis and phenotypic plasticity of the fungus across a range of controlled environments. In general, effects on plasticity are specific to an environment and mechanism, indicating that epigenetic regulation is context dependent and is not governed by general plasticity genes. Specifically, we found that, in Neurospora, histone methylation at H3K36 affected plastic response to high temperatures, H3K4 methylation affected plastic response to pH, but H3K27 methylation had no effect. Similarly, DNA methylation had only a small effect in response to sucrose. Histone deacetylation mainly decreased reaction norm elevation, as did genes involved in histone demethylation and acetylation. In contrast, the RNA interference pathway was involved in plastic responses to multiple environments.


2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Heidi S. Fisher ◽  
Emily Jacobs-Palmer ◽  
Jean-Marc Lassance ◽  
Hopi E. Hoekstra

1993 ◽  
Vol 115 (1) ◽  
pp. 89-94 ◽  
Author(s):  
K. T. Kim ◽  
Y. S. Kwon

Elastic-plastic responses of porous iron under uniaxial strain cycling between two fixed values of strain are investigated. A special set of constitutive equations is formulated by including isotropic, kinematic and saturation hardening responses. The theoretical results from the constitutive equations are compared with experimental cyclic data for porous iron, with various porosities.


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