scholarly journals Indirect Genetic Effects and the Spread of Infectious Disease: Are We Capturing the Full Heritable Variation Underlying Disease Prevalence?

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e39551 ◽  
Author(s):  
Debby Lipschutz-Powell ◽  
John A. Woolliams ◽  
Piter Bijma ◽  
Andrea B. Doeschl-Wilson
Keyword(s):  
Infectious Disease ◽  
Underlying Disease ◽  
Disease Prevalence ◽  
Genetic Effects ◽  
Heritable Variation ◽  
Indirect Genetic Effects

scholarly journals Indirect genetic effects underlie oxygen-limited thermal tolerance within a coastal population of chinook salmon

2014 ◽  
Vol 281 (1789) ◽  
pp. 20141082 ◽  
Author(s):  
Nicolas J. Muñoz ◽  
Katja Anttila ◽  
Zhongqi Chen ◽  
John W. Heath ◽  
Anthony P. Farrell ◽  
...  
Keyword(s):  
Maternal Effects ◽  
Chinook Salmon ◽  
Thermal Tolerance ◽  
Egg Size ◽  
Oncorhynchus Tshawytscha ◽  
Genetic Effects ◽  
Adaptation To Climate Change ◽  
Evolutionary Potential ◽  
Heritable Variation ◽  
Indirect Genetic Effects

With global temperatures projected to surpass the limits of thermal tolerance for many species, evaluating the heritable variation underlying thermal tolerance is critical for understanding the potential for adaptation to climate change. We examined the evolutionary potential of thermal tolerance within a population of chinook salmon ( Oncorhynchus tshawytscha ) by conducting a full-factorial breeding design and measuring the thermal performance of cardiac function and the critical thermal maximum (CT max ) of offspring from each family. Additive genetic variation in offspring phenotype was mostly negligible, although these direct genetic effects explained 53% of the variation in resting heart rate ( f H ). Conversely, maternal effects had a significant influence on resting f H , scope for f H , cardiac arrhythmia temperature and CT max . These maternal effects were associated with egg size, as indicated by strong relationships between the mean egg diameter of mothers and offspring thermal tolerance. Because egg size can be highly heritable in chinook salmon, our finding indicates that the maternal effects of egg size constitute an indirect genetic effect contributing to thermal tolerance. Such indirect genetic effects could accelerate evolutionary responses to the selection imposed by rising temperatures and could contribute to the population-specific thermal tolerance that has recently been uncovered among Pacific salmon populations.

scholarly journals The quantitative genetics of the endemic prevalence of infectious diseases: Indirect Genetic Effects dominate heritable variation and response to selection

2021 ◽  
Author(s):  
Piter Bijma ◽  
Andries Hulst ◽  
Mart C. M. de Jong
Keyword(s):  
Infectious Disease ◽  
Infectious Diseases ◽  
Disease Status ◽  
Host Population ◽  
Genetic Effects ◽  
Breeding Value ◽  
Response To Selection ◽  
Heritable Variation ◽  
Genetic Theory ◽  
Quantitative Genetic

AbstractPathogens have profound effects on life on earth, both in nature and agriculture. Despite the availability of well-established epidemiological theory, however, a quantitative genetic theory of the host population for the endemic prevalence of infectious diseases is almost entirely lacking. While several studies have demonstrated the relevance of the transmission dynamics of infectious diseases for heritable variation and response to selection of the host population, our current theoretical framework of quantitative genetics does not include these dynamics. As a consequence, we do not know which genetic effects of the host population determine the prevalence of an infectious disease, and have no concepts of breeding value and heritable variation for endemic prevalence.Here we propose a quantitative genetic theory for the endemic prevalence of infectious diseases. We first identify the genetic factors that determine the prevalence of an infectious disease, using an approach founded in epidemiological theory. Subsequently we investigate the population level effects of individual genetic variation on R0 and on the endemic prevalence. Next, we present expressions for the breeding value and heritable variation, for both prevalence and individual binary disease status, and show how these parameters depend on the endemic prevalence. Results show that heritable variation for endemic prevalence is substantially greater than currently believed, and increases when prevalence approaches zero, while heritability of individual disease status goes to zero. We show that response of prevalence to selection accelerates considerably when prevalence goes down, in contrast to predictions based on classical genetic models. Finally, we show that most of the heritable variation in the endemic prevalence of the infection is due to indirect genetic effects, suggestion a key role for kin-group selection both in the evolutionary history of current populations and for genetic improvement strategies in animals and plants.

scholarly journals Analysis of direct and indirect genetic effects in fighting sea anemones

2020 ◽  
Vol 31 (2) ◽  
pp. 540-547
Author(s):  
Sarah M Lane ◽  
Alastair J Wilson ◽  
Mark Briffa
Keyword(s):  
Individual Variation ◽  
Theoretical Models ◽  
Molecular Data ◽  
Genetic Effects ◽  
Sea Anemones ◽  
Heritable Variation ◽  
Evolutionarily Stable Strategies ◽  
Fighting Behavior ◽  
Indirect Genetic Effects

Abstract Theoretical models of animal contests such as the Hawk-Dove game predict that variation in fighting behavior will persist due to mixed evolutionarily stable strategies (ESS) under certain conditions. However, the genetic basis for this variation is poorly understood and a mixed ESS for fighting can be interpreted in more than one way. Specifically, we do not know whether variation in aggression within a population arises from among-individual differences in fixed strategy (determined by an individual’s genotype—direct genetic effects [DGEs]), or from within-individual variation in strategy across contests. Furthermore, as suggested by developments of the original Hawk-Dove model, within-individual variation in strategy may be dependent on the phenotype and thus genotype of the opponent (indirect genetic effects—IGEs). Here we test for the effect of DGEs and IGEs during fights in the beadlet sea anemone Actinia equina. By exploiting the unusual reproductive system of sea anemones, combined with new molecular data, we investigate the role of both additive (DGE + IGE) and non-additive (DGE × IGE) genetic effects on fighting parameters, the latter of which have been hypothesized but never tested for explicitly. We find evidence for heritable variation in fighting ability and that fight duration increases with relatedness. Fighting success is influenced additively by DGEs and IGEs but we found no evidence for non-additive IGEs. These results indicate that variation in fighting behavior is driven by additive indirect genetic effects (DGE + IGE), and support a core assumption of contest theory that strategies are fixed by DGEs.

scholarly journals Indirect genetic effects and the evolution of aggression in a vertebrate system

2008 ◽  
Vol 276 (1656) ◽  
pp. 533-541 ◽  
Author(s):  
Alastair J Wilson ◽  
Uriel Gelin ◽  
Marie-Claude Perron ◽  
Denis Réale
Keyword(s):  
Social Environment ◽  
Evolutionary Dynamics ◽  
Rapid Evolution ◽  
Genetic Effects ◽  
Deer Mice ◽  
Correlated Response ◽  
Experimental Population ◽  
Heritable Variation ◽  
Indirect Genetic Effects ◽  
The Social

Aggressive behaviours are necessarily expressed in a social context, such that individuals may be influenced by the phenotypes, and potentially the genotypes, of their social partners. Consequently, it has been hypothesized that indirect genetic effects (IGEs) arising from the social environment will provide a major source of heritable variation on which selection can act. However, there has been little empirical scrutiny of this to date. Here we test this hypothesis in an experimental population of deer mice ( Peromyscus maniculatus ). Using quantitative genetic models of five aggression traits, we find repeatable and heritable differences in agonistic behaviours of focal individuals when presented with an opponent mouse. For three of the traits, there is also support for the presence of IGEs, and estimated correlations between direct and indirect genetic ( rA O , F ) effects were high. As a consequence, any selection for aggression in the focal individuals should cause evolution of the social environment as a correlated response. In two traits, strong positive rA O , F will cause the rapid evolution of aggression, while in a third case changes in the phenotypic mean will be constrained by negative covariance between direct and IGEs. Our results illustrate how classical analyses may miss important components of heritable variation, and show that a full understanding of evolutionary dynamics requires explicit consideration of the genetic component of the social environment.

scholarly journals Belowground interactions shift the relative importance of direct and indirect genetic effects

2013 ◽  
Vol 3 (6) ◽  
pp. 1692-1701 ◽  
Author(s):  
Mark A. Genung ◽  
Joseph K. Bailey ◽  
Jennifer A. Schweitzer
Keyword(s):  
Genetic Effects ◽  
Relative Importance ◽  
Indirect Genetic Effects ◽  
Belowground Interactions

scholarly journals Indirect Genetic Effects and Housing Conditions in Relation to Aggressive Behaviour in Pigs

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e65136 ◽  
Author(s):  
Irene Camerlink ◽  
Simon P. Turner ◽  
Piter Bijma ◽  
J. Elizabeth Bolhuis
Keyword(s):  
Aggressive Behaviour ◽  
Genetic Effects ◽  
Housing Conditions ◽  
Indirect Genetic Effects

scholarly journals Evaluating indirect genetic effects of siblings using singletons

2021 ◽  
Author(s):  
Laurence Howe ◽  
David Evans ◽  
Gibran Hemani ◽  
George Davey Smith ◽  
Neil Martin Davies
Keyword(s):  
Genetic Variation ◽  
Educational Attainment ◽  
Family Environment ◽  
Phenotypic Variation ◽  
Molecular Genetic ◽  
Genetic Effects ◽  
Polygenic Risk Score ◽  
Indirect Genetic Effects ◽  
Molecular Genetic Evidence ◽  
Older Siblings

Estimating effects of parental and sibling genotypes (indirect genetic effects) can provide insight into how the family environment influences phenotypic variation. There is growing molecular genetic evidence for effects of parental phenotypes on their offspring (e.g. parental educational attainment), but the extent to which siblings affect each other is currently unclear.Here we used data from samples of unrelated individuals, without (singletons) and with biological full-siblings (non-singletons), to investigate and estimate sibling effects. Indirect genetic effects of siblings increase (or decrease) the covariance between genetic variation and a phenotype. It follows that differences in genetic association estimates between singletons and non-singletons could indicate indirect genetic effects of siblings.We used UK Biobank data to estimate polygenic risk score (PRS) associations for height, BMI and educational attainment in singletons (N = 50,143) and non-singletons (N = 328,549). The educational attainment PRS association estimate was 12% larger (95% C.I. 3%, 21%) in the non-singleton sample than in the singleton sample, but the height and BMI PRS associations were consistent. Birth order data suggested that the difference in educational attainment PRS associations was driven by individuals with older siblings rather than firstborns. The relationship between number of siblings and educational attainment PRS associations was non-linear; PRS associations were 24% smaller in individuals with 6 or more siblings compared to the rest of the sample (95% C.I. 11%, 38%). We estimate that a 1 SD increase in sibling educational attainment PRS corresponds to a 0.025 year increase in the index individual’s years in schooling (95% C.I. 0.013, 0.036).Our results suggest that older siblings influence the educational attainment of younger siblings, adding to the growing evidence that effects of the environment on phenotypic variation partially reflect social effects of germline genetic variation in relatives.

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