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Large effect loci often contain genes with critical developmental functions and potentially broad effects across life stages. However, their life stage-specific fitness consequences are rarely explored. In Atlantic salmon, variation in two large-effect loci, six6 and vgll3 , is linked to age at maturity and several physiological and behavioral traits in early life. By genotyping the progeny of wild Atlantic salmon that were planted into natural streams with nutrient manipulations, we tested if genetic variation in these loci is associated with survival in early life. We found that higher early-life survival was linked to the genotype associated with late maturation in the vgll3 , but with early maturation in the six6 locus. These effects were significant in high nutrients but not in low-nutrient streams. The differences in early survival were not explained by additive genetic effects in the offspring generation but by maternal genotypes in the six6 locus and by both parents' genotypes in the vgll3 locus. Our results suggest that indirect genetic effects of large-effect loci can be significant determinants of offspring fitness. This study demonstrates an intriguing case of how large-effect loci can exhibit complex fitness associations across life stages in the wild and indicates that predicting evolutionary dynamics is difficult. [ABSTRACT FROM AUTHOR]

Genetic mosaicism has long been linked to aging, and several hypotheses have been proposed to explain the potential connections between mosaicism and susceptibility to cancer. It has been proposed that mosaicism may disrupt tissue homeostasis by affecting intercellular communications and releasing microenvironmental constraints within tissues. The underlying mechanisms driving these tissue‐level influences remain unidentified, however. Here, we present an evolutionary perspective on the interplay between mosaicism and cancer, suggesting that the tissue‐level impacts of genetic mosaicism can be attributed to Indirect Genetic Effects (IGEs). IGEs can increase the level of cellular stochasticity and phenotypic instability among adjacent cells, thereby elevating the risk of cancer development within the tissue. Moreover, as cells experience phenotypic changes in response to challenging microenvironmental conditions, these changes can initiate a cascade of nongenetic alterations, referred to as Indirect non‐Genetic Effects (InGEs), which in turn catalyze IGEs among surrounding cells. We argue that incorporating both InGEs and IGEs into our understanding of the process of oncogenic transformation could trigger a major paradigm shift in cancer research with far‐reaching implications for practical applications. [ABSTRACT FROM AUTHOR]

Group size is an important trait for many ecological and evolutionary processes. However, it is not a trait possessed by individuals but by social groups, and as many genomes contribute to group size understanding its genetic underpinnings and so predicting its evolution is a conceptual challenge. Here I suggest how group size can be modelled as a joint phenotype of multiple individuals, and so how models for evolution accounting for indirect genetic effects are essential for understanding the genetic variance of group size. This approach makes it clear that (a) group size should have a larger genetic variance than initially expected as indirect genetic effects always contribute exactly as much as direct genetic effects and (b) the response to selection of group size should be faster than expected based on direct genetic variance alone as the correlation between direct and indirect effects is always at the maximum positive limit of 1. Group size should therefore show relatively rapid evolved increases and decreases, the consequences of which and evidence for I discuss. [ABSTRACT FROM AUTHOR]

Personality in non-human animals has been a popular area of research; however, it is still unknown how genetic and non-genetic factors influence the development of personality in many species. Therefore, we investigated how maternal genetic and non-genetic effects influenced adult offspring personality (exploration and anxiety) in the fawn-footed mosaic-tailed rat Melomys cervinipes. We first measured the amount of maternal care mothers provided to their offspring. Later, we assessed mothers and adult offspring over two testing sessions for exploratory behaviour using open field and novel object tests, and anxiety behaviour in a light/dark test. We calculated repeatability of behaviours and used parent–offspring regressions to assess heritability of behaviours. No measure of maternal care significantly influenced offspring personality. However, exploration of new spaces was constrained by maternal genetic effects. In contrast, anxiety and exploration of novel objects was more flexible, suggesting these behaviours may be more influenced by an individual's experiences during development. [ABSTRACT FROM AUTHOR]

The social environment is often the most dynamic and fitness-relevant environment animals experience. Here we tested whether plasticity arising from variation in social environments can promote signal-preference divergence—a key prediction of recent speciation theory but one that has proven difficult to test in natural systems. Interactions in mixed social aggregations could reduce, create, or enhance signal-preference differences. In the latter case, social plasticity could establish or increase assortative mating. We tested this by rearing two recently diverged species of Enchenopa treehoppers—sap-feeding insects that communicate with plant-borne vibrational signals—in treatments consisting of mixed-species versus own-species aggregations. Social experience with heterospecifics (in the mixed-species treatment) resulted in enhanced signal-preference species differences. For one of the two species, we tested but found no differences in the plastic response between sympatric and allopatric sites, suggesting the absence of reinforcement in the signals and preferences and their plastic response. Our results support the hypothesis that social plasticity can create or enhance signal-preference differences and that this might occur in the absence of long-term selection against hybridization on plastic responses themselves. Such social plasticity may facilitate rapid bursts of diversification. [ABSTRACT FROM AUTHOR]

The question of why females engage in extra-pair behaviors is long-standing in evolutionary biology. One suggestion is that these behaviors are maintained through pleiotropic effects on male extra-pair behaviors (genes controlling extra-pair reproduction are shared between sexes, but only beneficial to one sex, in this case, males). However, for this to evolve extra-pair reproduction must be both heritable and positively genetically correlated between sexes. Previous studies have suggested low heritability with no evidence for between-sex genetic correlations in extra-pair reproduction. However, these have not considered indirect genetic effects (derived from the behavior of others, IGEs) from the social partner, the influence of the social partner's genotype on the phenotype of an individual, despite the potential of IGEs to uncover hidden heritable variation. Using data from a closed-house sparrow population with a genetic pedigree spanning two decades, we tested the influence of social partner IGEs on heritable variation and genetic correlation estimates of extra-pair reproduction. We found that the inclusion of IGEs resulted in larger heritable genetic variance for both male and female extra-pair heritability. While IGEs did not change between-sex genetic correlations, we found they reduced uncertainty in those estimates. Future studies should consider the effect of IGEs on the mechanisms of sex-specific extra-pair reproduction. [ABSTRACT FROM AUTHOR]

Affiliative social behaviors are linked to fitness components in multiple species. However, the role of genetic variance in shaping such behaviors remains largely unknown, limiting our understanding of how affiliative behaviors can respond to natural selection. Here, we employed the "animal model" to estimate environmental and genetic sources of variance and covariance in grooming behavior in the well-studied Amboseli wild baboon population. We found that the tendency for a female baboon to groom others ("grooming given") is heritable (h 2 = 0.22 ± 0.048), and that several environmental variables—including dominance rank and the availability of kin as grooming partners—contribute to variance in this grooming behavior. We also detected small but measurable variance due to the indirect genetic effect of partner identity on the amount of grooming given within dyadic grooming partnerships. The indirect and direct genetic effects for grooming given were positively correlated (r = 0.74 ± 0.09). Our results provide insight into the evolvability of affiliative behavior in wild animals, including the possibility for correlations between direct and indirect genetic effects to accelerate the response to selection. As such they provide novel information about the genetic architecture of social behavior in nature, with important implications for the evolution of cooperation and reciprocity. [ABSTRACT FROM AUTHOR]

Indirect genetic effects describe phenotypic variation that results from differences in the genotypic composition of social partners. Such effects represent heritable sources of environmental variation in eusocial organisms because individuals are typically reared by their siblings. In the fire ant Solenopsis invicta, a social supergene exhibits striking indirect genetic effects on worker regulation of colony queen number, such that the genotypic composition of workers at the supergene determines whether colonies contain a single or multiple queens. We assessed the direct and indirect genetic effects of this supergene on gene expression in brains and abdominal tissues from laboratory‐reared workers and compared these with previously published data from field‐collected prereproductive queens. We found that direct genetic effects caused larger gene expression changes and were more consistent across tissue types and castes than indirect genetic effects. Indirect genetic effects influenced the expression of many loci but were generally restricted to the abdominal tissues. Further, indirect genetic effects were only detected when the genotypic composition of social partners differed throughout the development and adult life of focal workers, and were often only significant with relatively lenient statistical cutoffs. Our study provides insight into direct and indirect genetic effects of a social supergene on gene regulatory dynamics across tissues and castes in a complex society. [ABSTRACT FROM AUTHOR]

In mutualism, hosts select symbionts via partner choice and preferentially direct more resources to symbionts that provide greater benefits via sanctions. At the initiation of symbiosis, prior to resource exchange, it is not known how the presence of multiple symbiont options (i.e. the symbiont social environment) impacts partner choice outcomes. Furthermore, little research addresses whether hosts primarily discriminate among symbionts via sanctions, partner choice or a combination. We inoculated the legume, Acmispon wrangelianus, with 28 pairs of fluorescently labelled Mesorhizobium strains that vary continuously in quality as nitrogen-fixing symbionts. We find that hosts exert robust partner choice, which enhances their fitness. This partner choice is conditional such that a strain's success in initiating nodules is impacted by other strains in the social environment. This social genetic effect is as important as a strain's own genotype in determining nodulation and has both transitive (consistent) and intransitive (idiosyncratic) effects on the probability that a symbiont will form a nodule. Furthermore, both absolute and conditional partner choice act in concert with sanctions, among and within nodules. Thus, multiple forms of host discrimination act as a series of sieves that optimize host benefits and select for costly symbiont cooperation in mixed symbiont populations. [ABSTRACT FROM AUTHOR]

The decision to leave or join a group is important as group size influences many aspects of organisms' lives and their fitness. This tendency to socialise with others, sociability, should be influenced by genes carried by focal individuals (direct genetic effects) and by genes in partner individuals (indirect genetic effects), indicating the trait's evolution could be slower or faster than expected. However, estimating these genetic parameters is difficult. Here, in a laboratory population of the cockroach Blaptica dubia, I estimate phenotypic parameters for sociability: repeatability (R) and repeatable influence (RI), that indicate whether direct and indirect genetic effects respectively are likely. I also estimate the interaction coefficient (Ψ), which quantifies how strongly a partner's trait influences the phenotype of the focal individual and is key in models for the evolution of interacting phenotypes. Focal individuals were somewhat repeatable for sociability across a 3‐week period (R = 0.080), and partners also had marginally consistent effects on focal sociability (RI = 0.053). The interaction coefficient was non‐zero, although in opposite sign for the sexes; males preferred to associate with larger individuals (Ψmale = −0.129), while females preferred to associate with smaller individuals (Ψfemale = 0.071). Individual sociability was consistent between dyadic trials and in social networks of groups. These results provide phenotypic evidence that direct and indirect genetic effects have limited influence on sociability, with perhaps most evolutionary potential stemming from heritable effects of the body mass of partners. Sex‐specific interaction coefficients may produce sexual conflict and the evolution of sexual dimorphism in social behaviour. [ABSTRACT FROM AUTHOR]

Abstract Phenotypic variability of a genotype is relevant both in natural and domestic populations. In the past two decades, variability has been studied as a heritable quantitative genetic trait in its own right, often referred to as inherited variability or environmental canalization. So far, studies on inherited variability have only considered genetic effects of the focal individual, that is, direct genetic effects on inherited variability. Observations from aquaculture populations and some plants, however, suggest that an additional source of genetic variation in inherited variability may be generated through competition. Social interactions, such as competition, are often a source of Indirect Genetic Effects (IGE). An IGE is a heritable effect of an individual on the trait value of another individual. IGEs may substantially affect heritable variation underlying the trait, and the direction and magnitude of response to selection. To understand the contribution of IGEs to evolution of environmental canalization in natural populations, and to exploit such inherited variability in animal and plant breeding, we need statistical models to capture this effect. To our knowledge, it is unknown to what extent the current statistical models commonly used for IGE and inherited variability capture the effect of competition on inherited variability. Here, we investigate the potential of current statistical models for inherited variability and trait values, to capture the direct and indirect genetic effects of competition on variability. Our results show that a direct model of inherited variability almost entirely captures the genetic sensitivity of individuals to competition, whereas an indirect model of inherited variability captures the cooperative genetic effects of individuals on their partners. Models for trait levels, however, capture only a small part of the genetic effects of competition. The estimation of direct and indirect genetic effects of competition, therefore, is possible with models for inherited variability but may require a two‐step analysis.

Genes not only control traits of their carrier organism (known as direct genetic effects or DGEs) but also shape their carrier's physical environment and the phenotypes of their carrier's social partners (known as indirect genetic effects or IGEs). Theoretical research has shown that the effects that genes exert on social partners can have profound consequences, potentially altering heritability and the direction of trait evolution. Complementary empirical research has shown that in various contexts (particularly in animal agriculture) IGEs can explain a large proportion of variation in specific traits. However, little is known about the general prevalence of IGEs. We conducted a reciprocal cross‐fostering experiment with two genetic lineages of the clonal raider ant Ooceraea biroi to quantify the relative contribution of DGEs and IGEs to variation in brain gene expression (which underlies behavioural variation). We found that thousands of genes are differentially expressed by DGEs but not a single gene is differentially expressed by IGEs. This is surprising given the highly social context of ant colonies and given that individual behaviour varies according to the genotypic composition of the social environment in O. biroi. Overall, these findings indicate that we have a lot to learn about how the magnitude of IGEs varies across species and contexts. [ABSTRACT FROM AUTHOR]

In natural populations, quantitative traits seldom show short‐term evolution at the rate predicted by evolutionary models. Resolving this "paradox of stasis" is a key goal in evolutionary biology, as it directly challenges our capacity to predict evolutionary change. One particularly promising hypothesis to explain the lack of evolutionary responses in a key offspring trait, body weight, is that positive selection on juveniles is counterbalanced by selection against maternal investment in offspring growth, given that reproduction is costly for the mothers. Here, we used data from one of the longest individual‐based studies of a wild mammal population to test this hypothesis. We first showed that despite positive directional selection on birth weight, and heritable variation for this trait, no genetic change has been observed for birth weight over the past 47 years in the study population. Contrarily to our expectation, we found no evidence of selection against maternal investment in birth weight—if anything, selection favors mothers that produce large calves. Accordingly, we show that genetic change in birth weight over the study period is actually lower than that predicted from models including selection on maternal performance; ultimately our analysis here only deepens rather than resolves the paradox of stasis. [ABSTRACT FROM AUTHOR]

Background: Theoretical models of the development of childhood externalizing disorders emphasize the role of parents. Empirical studies have not been able to identify specific aspects of parental behaviors explaining a considerable proportion of the observed individual differences in externalizing problems. The problem is complicated by the contribution of genetic factors to externalizing problems, as parents provide both genes and environments to their children. We studied the joint contributions of direct genetic effects of children and the indirect genetic effects of parents through the environment on externalizing problems. Methods: The study used genome‐wide single nucleotide polymorphism data from 9,675 parent–offspring trios participating in the Norwegian Mother Father and child cohort study. Based on genomic relatedness matrices, we estimated the contribution of direct genetic effects and indirect maternal and paternal genetic effects on ADHD, conduct and disruptive behaviors at 8 years of age. Results: Models including indirect parental genetic effects were preferred for the ADHD symptoms of inattention and hyperactivity, and conduct problems, but not oppositional defiant behaviors. Direct genetic effects accounted for 11% to 24% of the variance, whereas indirect parental genetic effects accounted for 0% to 16% in ADHD symptoms and conduct problems. The correlation between direct and indirect genetic effects, or gene–environment correlations, decreased the variance with 16% and 13% for conduct and inattention problems, and increased the variance with 6% for hyperactivity problems. Conclusions: This study provides empirical support to the notion that parents have a significant role in the development of childhood externalizing behaviors. The parental contribution to decrease in variation of inattention and conduct problems by gene–environment correlations would limit the number of children reaching clinical ranges in symptoms. Not accounting for indirect parental genetic effects can lead to both positive and negative bias when identifying genetic variants for childhood externalizing behaviors. [ABSTRACT FROM AUTHOR]

Variability in warning signals is common but remains puzzling since deviations from the most common form should result in a higher number of predator attacks. One explanation may lie in constraints due to genetic correlations between warning colour and other traits under selection. To explore the relationship between variation in warning colour and different life-history traits, we used an extensive data set comprising 64,741 individuals from a Finnish and an Estonian population of the wood tiger moths, Arctia plantaginis, that have been maintained in captivity over 25 generations. This species exhibits variable warning coloration in larval and adult stages. Measuring these traits alongside several fitness components allowed us to set colour variation into context and obtain a better understanding of selection and constraints. Complete pedigree information enabled us to estimate genetic variances and covariances, which revealed several complex interplays between fitness components: Selection for faster development led to a significantly reduced fecundity. Fecundity was also constrained by negative correlations between direct genetic and maternal effects. However, we found no evidence that genetic associations with life-history traits constrain efficiency of warning colours., (© The Author(s) 2024. Published by Oxford University Press on behalf of The Society for the Study of Evolution (SSE).)

Abstract There is tantalizing evidence that phenotypic plasticity can buffer novel, adaptive genetic variants long enough to permit their evolutionary spread, and this process is often invoked in explanations for rapid adaptive evolution. However, the strength and generality of evidence for it is controversial. We identify a conceptual problem affecting this debate: recombination, segregation, and independent assortment are expected to quickly sever associations between genes controlling novel adaptations and genes contributing to trait plasticity that facilitates the novel adaptations by reducing their indirect fitness costs. To make clearer predictions about this role of plasticity in facilitating genetic adaptation, we describe a testable genetic mechanism that resolves the problem: genetic covariance between new adaptive variants and trait plasticity that facilitates their persistence within populations. We identify genetic architectures that might lead to such a covariance, including genetic coupling via physical linkage and pleiotropy, and illustrate the consequences for adaptation rates using numerical simulations. Such genetic covariances may also arise from the social environment, and we suggest the indirect genetic effects that result could further accentuate the process of adaptation. We call the latter mechanism of adaptation social drive, and identify methods to test it. We suggest that genetic coupling of plasticity and adaptations could promote unusually rapid ‘runaway’ evolution of novel adaptations. The resultant dynamics could facilitate evolutionary rescue, adaptive radiations, the origin of novelties, and other commonly studied processes.

Abstract Background The phenotype of an individual can be affected not only by the individual’s own genotypes, known as direct genetic effects (DGE), but also by genotypes of interacting partners, indirect genetic effects (IGE). IGE have been detected using polygenic models in multiple species, including laboratory mice and humans. However, the underlying mechanisms remain largely unknown. Genome-wide association studies of IGE (igeGWAS) can point to IGE genes, but have not yet been applied to non-familial IGE arising from “peers” and affecting biomedical phenotypes. In addition, the extent to which igeGWAS will identify loci not identified by dgeGWAS remains an open question. Finally, findings from igeGWAS have not been confirmed by experimental manipulation. Results We leverage a dataset of 170 behavioral, physiological, and morphological phenotypes measured in 1812 genetically heterogeneous laboratory mice to study IGE arising between same-sex, adult, unrelated mice housed in the same cage. We develop and apply methods for igeGWAS in this context and identify 24 significant IGE loci for 17 phenotypes (FDR

Abstract Queens of eusocial species live extraordinarily long compared to their workers. So far, it has been argued that these lifespan divergences are readily explained by the classical evolutionary theory of ageing. As workers predominantly perform risky tasks, such as foraging and nest defense, and queens stay in the well‐protected nests, selection against harmful genetic mutations expressed in old age should be weaker in workers than in queens due to caste differences in extrinsic mortality risk, and thus, lead to the evolution of longer queen and shorter worker lifespans. However, these arguments have not been supported by formal models. Here, we present a model for the evolution of caste‐specific ageing in social insects, based on Williams’ antagonistic pleiotropy theory of ageing. In individual‐based simulations, we assume that mutations with antagonistic fitness effects can act within castes, that is, mutations in early life are accompanied by an antagonistic effect acting in later life, or between castes, where antagonistic effects emerge due to caste antagonism or indirect genetic effects between castes. In monogynous social insect species with sterile workers, large lifespan divergences between castes evolved under all different scenarios of antagonistic effects, but regardless of the degree of caste‐specific extrinsic mortality. Mutations with antagonistic fitness effects within castes reduced lifespans of both castes, while mutations with between‐caste antagonistic effects decreased worker lifespans more than queen lifespans, and consequently increased lifespan divergences. Our results challenge the central explanatory role of extrinsic mortality for caste‐specific ageing in eusocial organisms and suggest that antagonistic pleiotropy affects castes differently due to reproductive monopolization by queens, hence, reproductive division of labor. Finally, these findings provide new insights into the evolution of tissue‐specific ageing in multicellular organisms in general.

A central tenet of niche construction (NC) theory is that organisms can alter their environments in heritable and evolutionarily important ways, often altering selection pressures. We suggest that the physical changes niche constructors make to their environments may also alter trait heritability and the response of phenotypes to selection. This effect might change evolution, over and above the effect of NC acting via selection alone. We develop models of trait evolution that allow us to partition the effects of NC on trait heritability from those on selection to better investigate their distinct effects. We show that the response of a phenotype to selection and so the pace of phenotypic change can be considerably altered in the presence of NC and that this effect is compounded when trans-generational interactions are included. We argue that novel mathematical approaches are needed to describe the simultaneous effects of NC on trait evolution via selection and heritability. Just as indirect genetic effects have been shown to significantly increase trait heritability, the effects of NC on heritability in our model suggest a need for further theoretical development of the concept of heritability. [ABSTRACT FROM AUTHOR]

Phenotypic variability of a genotype is relevant both in natural and domestic populations. In the past two decades, variability has been studied as a heritable quantitative genetic trait in its own right, often referred to as inherited variability or environmental canalization. So far, studies on inherited variability have only considered genetic effects of the focal individual, that is, direct genetic effects on inherited variability. Observations from aquaculture populations and some plants, however, suggest that an additional source of genetic variation in inherited variability may be generated through competition. Social interactions, such as competition, are often a source of Indirect Genetic Effects (IGE). An IGE is a heritable effect of an individual on the trait value of another individual. IGEs may substantially affect heritable variation underlying the trait, and the direction and magnitude of response to selection. To understand the contribution of IGEs to evolution of environmental canalization in natural populations, and to exploit such inherited variability in animal and plant breeding, we need statistical models to capture this effect. To our knowledge, it is unknown to what extent the current statistical models commonly used for IGE and inherited variability capture the effect of competition on inherited variability. Here, we investigate the potential of current statistical models for inherited variability and trait values, to capture the direct and indirect genetic effects of competition on variability. Our results show that a direct model of inherited variability almost entirely captures the genetic sensitivity of individuals to competition, whereas an indirect model of inherited variability captures the cooperative genetic effects of individuals on their partners. Models for trait levels, however, capture only a small part of the genetic effects of competition. The estimation of direct and indirect genetic effects of competition, therefore, is possible with models for inherited variability but may require a two‐step analysis. [ABSTRACT FROM AUTHOR]

Abstract We investigate the evolution of a gene for paternal care, with pleiotropic effects on male mating fitness and offspring viability, with and without extrapair copulations (EPCs). We develop a population genetic model to examine how pleiotropic effects of a male mating advantage and paternal care are affected by “good genes” and EPCs. Using this approach, we show that the relative effects of each on fitness do not always predict the evolutionary change. We then find the line of combinations of mating success and paternal care that bisects the plane of possible values into regions of positive or negative gene frequency change. This line shifts when either good genes or EPCs are introduced, thereby expanding or contracting the region of positive gene frequency change and significantly affecting the evolution of paternal care. Predictably, a direct viability effect of “good genes” that enhances offspring viability constrains or expands the parameter space over which paternal care can evolve, depending on whether the viability effect is associated with the paternal care allele or not. In either case, the effect of a “good gene” that enhances offspring viability is substantial; when strong enough, it can even facilitate the evolution of poor paternal care, where males harm their young. When nonrandom mating is followed by random EPCs, the genetic regression between sire and offspring is reduced and, consequently, the relative strengths of selection are skewed away from paternal care and toward the male mating advantage. However, when random mating is followed by nonrandom EPCs, a situation called “trading up” by females, we show that selection is skewed in the opposite direction, away from male mating advantage and toward paternal care across the natural range of EPC frequencies.

Wondrously elaborate weapons and displays that appear to be counter to ecological optima are widespread features of male contests for mates across the animal kingdom. To understand how such diverse traits evolve, here we develop a quantitative genetic model of sexual selection for a male signaling trait that mediates aggression in male‐male contests and show that an honest indicator of aggression can generate selection on itself by altering the social environment. This can cause selection to accelerate as the trait is elaborated, leading to runaway evolution. Thus, an evolving source of selection provided by the social environment is the fundamental unifying feature of runaway sexual selection driven by either male‐male competition or female mate choice. However, a key difference is that runaway driven by male‐male competition requires signal honesty. Our model identifies simple conditions that provide clear, testable predictions for empirical studies using standard quantitative genetic methods. [ABSTRACT FROM AUTHOR]

Infectious diseases have profound effects on life, both in nature and agriculture. 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 transmission of infections for heritable variation and response to selection, current quantitative genetics ignores transmission. Thus, we lack concepts of breeding value and heritable variation for endemic prevalence, and poorly understand response of endemic prevalence to selection. Here, we integrate quantitative genetics and epidemiology, and propose a quantitative genetic theory for the basic reproduction number R0 and for the endemic prevalence of an infection. We first identify the genetic factors that determine the prevalence. Subsequently, we investigate the population-level consequences of individual genetic variation, for both R0 and the endemic prevalence. Next, we present expressions for the breeding value and heritable variation, for endemic prevalence and individual binary disease status, and show that these depend strongly on the prevalence. Results show that heritable variation for endemic prevalence is substantially greater than currently believed, and increases strongly when prevalence decreases, while heritability of disease status approaches zero. As a consequence, response of the endemic prevalence to selection for lower disease status accelerates considerably when prevalence decreases, in contrast to classical predictions. Finally, we show that most heritable variation for the endemic prevalence is hidden in indirect genetic effects, suggesting a key role for kin-group selection in the evolutionary history of current populations and for genetic improvement in animals and plants. [ABSTRACT FROM AUTHOR]

Two popular approaches for modeling social evolution, evolutionary game theory and quantitative genetics, ask complementary questions but are rarely integrated. Game theory focuses on evolutionary outcomes, with models solving for evolutionarily stable equilibria, whereas quantitative genetics provides insight into evolutionary processes, with models predicting short-term responses to selection. Here we draw parallels between evolutionary game theory and interacting phenotypes theory, which is a quantitative genetic framework for understanding social evolution. First, we show how any evolutionary game may be translated into two quantitative genetic selection gradients, nonsocial and social selection, which may be used to predict evolutionary change from a single round of the game. We show that synergistic fitness effects may alter predicted selection gradients, causing changes in magnitude and sign as the population mean evolves. Second, we show how evolutionary games involving plastic behavioral responses to partners can be modeled using indirect genetic effects, which describe how trait expression changes in response to genes in the social environment. We demonstrate that repeated social interactions in models of reciprocity generate indirect effects and conversely, that estimates of parameters from indirect genetic effect models may be used to predict the evolution of reciprocity. We argue that a pluralistic view incorporating both theoretical approaches will benefit empiricists and theorists studying social evolution. We advocate the measurement of social selection and indirect genetic effects in natural populations to test the predictions from game theory and, in turn, the use of game theory models to aid in the interpretation of quantitative genetic estimates. [ABSTRACT FROM AUTHOR]

Social interactions with conspecifics can dramatically affect an individual's fitness. The positive or negative consequences of interacting with social partners typically depend on the value of traits that they express. These pathways of social selection connect the traits and genes expressed in some individuals to the fitness realized by others, thereby altering the total phenotypic selection on and evolutionary response of traits across the multivariate phenotype. The downstream effects of social selection are mediated by the patterns of phenotypic assortment between focal individuals and their social partners (the interactant covariance, C i j ′ ⁠ , or the multivariate form, C I). Depending on the sign and magnitude of the interactant covariance, the direction of social selection can be reinforced, reversed, or erased. We report estimates of C i j ′ from a variety of studies of forked fungus beetles to address the largely unexplored questions of consistency and plasticity of phenotypic assortment in natural populations. We found that phenotypic assortment of male beetles based on body size or horn length was highly variable among subpopulations, but that those differences also were broadly consistent from year to year. At the same time, the strength and direction of C i j ′ changed quickly in response to experimental changes in resource distribution and social properties of populations. Generally, interactant covariances were more negative in contexts in which the number of social interactions was greater in both field and experimental situations. These results suggest that patterns of phenotypic assortment could be important contributors to variability in multilevel selection through their mediation of social selection gradients. [ABSTRACT FROM AUTHOR]

Evolution by natural selection is often viewed as a process that inevitably leads to adaptation or an increase in population fitness over time. However, maladaptation, an evolved decrease in fitness, may also occur in response to natural selection under some conditions. Social selection, which arises from the effects of social partners on fitness, has been identified as a potential cause of maladaptation, but we lack a general rule identifying when social selection should lead to a decrease in population mean fitness. Here we use a quantitative genetic model to develop such a rule. We show that maladaptation is most likely to occur when social selection is strong relative to nonsocial selection and acts in an opposing direction. In this scenario, the evolution of traits that impose fitness costs on others may outweigh evolved gains in fitness for the individual, leading to a net decrease in population mean fitness. Furthermore, we find that maladaptation may also sometimes occur when phenotypes of interacting individuals negatively covary. We outline the biological situations where maladaptation in response to social selection can be expected, provide both quantitative genetic and phenotypic versions of our derived result, and suggest what empirical work would be needed to test it. We also consider the effect of social selection on inclusive fitness and support previous work showing that inclusive fitness cannot suffer an evolutionary decrease. Taken together, our results show that social selection may decrease population mean fitness when it opposes individual-level selection, even as inclusive fitness increases. [ABSTRACT FROM AUTHOR]

We use population genetics to model the evolution of a gene with an indirect effect owing to paternal care and with a second pleiotropic, direct effect on offspring viability. We use the model to illustrate how the common empirical practice of considering offspring viability as a component of parent fitness can confound a gene's direct and indirect fitness effects. We investigate when this confounding results in a distorted picture of overall evolution and when it does not. We find that the practice has no effect on mean fitness, W, but it does have an effect on the dynamics of gene frequency change, ∆q. We also find that, for some regions of parameter space associated with fitness trade-offs, the distortion is not only quantitative but also qualitative, obscuring the direction of gene frequency change. Because it affects the evolutionary dynamics, it also affects the expected amount of genetic variation at mutation-selection balance, an important consideration in molecular evolution. We discuss empirical techniques for separating direct from indirect effects and how field studies measuring the value of male paternal care might be improved by using them. [ABSTRACT FROM AUTHOR]

When resources are limited, mean fitness is constrained and competition can cause genes and phenotypes to enhance an individual's own fitness while reducing the fitness of their competitors. Negative social effects on fitness have the potential to constrain adaptation, but the interplay between ecological opportunity and social constraints on adaptation remains poorly studied in nature. Here, we tested for evidence of phenotypic social effects on annual fitness (survival and reproductive success) in a long-term study of wild North American red squirrels (Tamiasciurus hudsonicus) under conditions of both resource limitation and super-abundant food resources. When resources were limited, populations remained stable or declined, and there were strong negative social effects on annual survival and reproductive success. That is, mean fitness was constrained and individuals had lower fitness when other nearby individuals had higher fitness. In contrast, when food resources were super-abundant, populations grew and social constraints on reproductive success were greatly reduced or eliminated. Unlike reproductive success, social constraints on survival were not significantly reduced when food resources were super-abundant. These findings suggest resource-dependent social constraints on a component of fitness, which have important potential implications for evolution and adaptation. [ABSTRACT FROM AUTHOR]

Evolvable traits of organisms can alter the environment those organisms experience. While it is well appreciated that those modified environments can influence natural selection to which organisms are exposed, they can also influence the expression of genetic variances and covariances of traits under selection. When genetic variance and covariance change in response to changes in the evolving, modified environment, rates and outcomes of evolution also change. Here we discuss the basic mechanisms whereby organisms modify their environments, review how those modified environments have been shown to alter genetic variance and covariance, and discuss potential evolutionary consequences of such dynamics. With these dynamics, responses to selection can be more rapid and sustained, leading to more extreme phenotypes, or they can be slower and truncated, leading to more conserved phenotypes. Patterns of correlated selection can also change, leading to greater or less evolutionary independence of traits, or even causing convergence or divergence of traits, even when selection on them is consistent across environments. Developing evolutionary models that incorporate changes in genetic variances and covariances when environments themselves evolve requires developing methods to predict how genetic parameters respond to environments—frequently multifactorial environments. It also requires a population-level analysis of how traits of collections of individuals modify environments for themselves and/or others in a population, possibly in spatially explicit ways. Despite the challenges of elucidating the mechanisms and nuances of these processes, even qualitative predictions of how environment-modifying traits alter evolutionary potential are likely to improve projections of evolutionary outcomes. [ABSTRACT FROM AUTHOR]

Maternal-zygotic co-evolution is one of the most common examples of indirect genetic effects. I investigate how maternal-zygotic gene interactions affect rates of evolution and adaptation. Using comparably parameterized population genetic models, I compare evolution to an abiotic environment with genotype-by-environment interaction (G × E) to evolution to a maternal environment with offspring genotype-by-maternal environment interaction (G × Gmaternal). There are strong parallels between the 2 models in the components of fitness variance but they differ in their rates of evolution measured in terms of ∆p, gene frequency change, or of ∆W, change in mean fitness. The Price Equation is used to partition ∆W into 2 components, one owing to the genetic variance in fitness by natural selection and a second owing to change in environment. Adaptive evolution is faster in the 2-locus model with G × Gmaternal with free recombination, than it is in the 1-locus model with G × E, because in the former the maternal genetic environment coevolves with the zygotic phenotype adapting to it. I discuss the relevance of these findings for the evolution of genes with indirect genetic effects. [ABSTRACT FROM AUTHOR]

Intercropping is both a well-established and yet novel agricultural practice, depending on one's perspective. Such perspectives are principally governed by geographic location and whether monocultural practices predominate. Given the negative environmental effects of monoculture agriculture (loss of biodiversity, reliance on non-renewable inputs, soil degradation, etc.), there has been a renewed interest in cropping systems that can reduce the impact of modern agriculture while maintaining (or even increasing) yields. Intercropping is one of the most promising practices in this regard, yet faces a multitude of challenges if it is to compete with and ultimately replace the prevailing monocultural norm. These challenges include the necessity for more complex agricultural designs in space and time, bespoke machinery, and adapted crop cultivars. Plant breeding for monocultures has focused on maximizing yield in single-species stands, leading to highly productive yet specialized genotypes. However, indications suggest that these genotypes are not the best adapted to intercropping systems. Re-designing breeding programs to accommodate inter-specific interactions and compatibilities, with potentially multiple different intercropping partners, is certainly challenging, but recent technological advances offer novel solutions. We identify a number of such technology-driven directions, either ideotype-driven (i.e., "trait-based" breeding) or quantitative genetics-driven (i.e., "product-based" breeding). For ideotype breeding, plant growth modeling can help predict plant traits that affect both inter- and intraspecific interactions and their influence on crop performance. Quantitative breeding approaches, on the other hand, estimate breeding values of component crops without necessarily understanding the underlying mechanisms. We argue that a combined approach, for example, integrating plant growth modeling with genomic-assisted selection and indirect genetic effects, may offer the best chance to bridge the gap between current monoculture breeding programs and the more integrated and diverse breeding programs of the future. [ABSTRACT FROM AUTHOR]

Complex problems in evolutionary biology can be approached in two ways, top down using theoretical constructs and bottom up using empirical studies. Theoretical concepts predominate evolutionary interpretations of eusociality in a literature that is small relative to an enormous literature of natural history and basic research that is not synthesized into a conceptual whole. Here, I draw insights from this literature to show how paper wasps' allomaternal non-reproductive worker phenotype originates in every colony cycle via confluence of multiple factors of paper wasp biology. These include behavior, development, nutrient dynamics, indirect genetic effects, sex ratio, and demography. A novel perspective on the colony cycle, based on individuals' reproductive physiology, serves as context to examine of each of these. It will be shown that the allomaternal non-reproductive worker phenotype does not require relatedness among colony members to originate. Allomaternal care of non-relatives is frequent and can occur in at least twelve contexts. Life histories of living species as they will be presented here show that relatedness among colony members is not the target of selection in simple eusociality. However, the novel allomaternal non-reproductive worker phenotype had to be present at the ancestral origins of complex eusociality in which relatedness among colony members is essential. [ABSTRACT FROM AUTHOR]

There is tantalizing evidence that phenotypic plasticity can buffer novel, adaptive genetic variants long enough to permit their evolutionary spread, and this process is often invoked in explanations for rapid adaptive evolution. However, the strength and generality of evidence for it is controversial. We identify a conceptual problem affecting this debate: recombination, segregation, and independent assortment are expected to quickly sever associations between genes controlling novel adaptations and genes contributing to trait plasticity that facilitates the novel adaptations by reducing their indirect fitness costs. To make clearer predictions about this role of plasticity in facilitating genetic adaptation, we describe a testable genetic mechanism that resolves the problem: genetic covariance between new adaptive variants and trait plasticity that facilitates their persistence within populations. We identify genetic architectures that might lead to such a covariance, including genetic coupling via physical linkage and pleiotropy, and illustrate the consequences for adaptation rates using numerical simulations. Such genetic covariances may also arise from the social environment, and we suggest the indirect genetic effects that result could further accentuate the process of adaptation. We call the latter mechanism of adaptation social drive, and identify methods to test it. We suggest that genetic coupling of plasticity and adaptations could promote unusually rapid 'runaway' evolution of novel adaptations. The resultant dynamics could facilitate evolutionary rescue, adaptive radiations, the origin of novelties, and other commonly studied processes. [ABSTRACT FROM AUTHOR]

The caste fate of developing female honey bee larvae is strictly socially regulated by adult nurse workers. As a result of this social regulation, nurse-expressed genes as well as larval-expressed genes may affect caste expression and evolution. We used a novel transcriptomic approach to identify genes with putative direct and indirect effects on honey bee caste development, and we subsequently studied the relative rates of molecular evolution at these caste-associated genes. We experimentally induced the production of new queens by removing the current colony queen, and we used RNA sequencing to study the gene expression profiles of both developing larvae and their caregiving nurses before and after queen removal. By comparing the gene expression profiles of queen-destined versus worker-destined larvae as well as nurses observed feeding these two types of larvae, we identified larval and nurse genes associated with caste development. Of 950 differentially expressed genes associated with caste, 82% were expressed in larvae with putative direct effects on larval caste, and 18% were expressed in nurses with putative indirect effects on caste. Estimated selection coefficients suggest that both nurse and larval genes putatively associated with caste are rapidly evolving, especially those genes associated with worker development. Altogether, our results suggest that indirect effect genes play important roles in both the expression and evolution of socially influenced traits such as caste.

Intercropping is both a well-established and yet novel agricultural practice, depending on one’s perspective. Such perspectives are principally governed by geographic location and whether monocultural practices predominate. Given the negative environmental effects of monoculture agriculture (loss of biodiversity, reliance on non-renewable inputs, soil degradation, etc.), there has been a renewed interest in cropping systems that can reduce the impact of modern agriculture while maintaining (or even increasing) yields. Intercropping is one of the most promising practices in this regard, yet faces a multitude of challenges if it is to compete with and ultimately replace the prevailing monocultural norm. These challenges include the necessity for more complex agricultural designs in space and time, bespoke machinery, and adapted crop cultivars. Plant breeding for monocultures has focused on maximizing yield in single-species stands, leading to highly productive yet specialized genotypes. However, indications suggest that these genotypes are not the best adapted to intercropping systems. Re-designing breeding programs to accommodate inter-specific interactions and compatibilities, with potentially multiple different intercropping partners, is certainly challenging, but recent technological advances offer novel solutions. We identify a number of such technology-driven directions, either ideotype-driven (i.e., “trait-based” breeding) or quantitative genetics-driven (i.e., “product-based” breeding). For ideotype breeding, plant growth modeling can help predict plant traits that affect both inter- and intraspecific interactions and their influence on crop performance. Quantitative breeding approaches, on the other hand, estimate breeding values of component crops without necessarily understanding the underlying mechanisms. We argue that a combined approach, for example, integrating plant growth modeling with genomic-assisted selection and indirect genetic effects, may offer the best chance to bridge the gap between current monoculture breeding programs and the more integrated and diverse breeding programs of the future.

Abstract The green‐beard effect is one proposed mechanism predicted to underpin the evolution of altruistic behavior. It relies on the recognition and the selective help of altruists to each other in order to promote and sustain altruistic behavior. However, this mechanism has often been dismissed as unlikely or uncommon, as it is assumed that both the signaling trait and altruistic trait need to be encoded by the same gene or through tightly linked genes. Here, we use models of indirect genetic effects (IGEs) to find the minimum correlation between the signaling and altruistic trait required for the evolution of the latter. We show that this correlation threshold depends on the strength of the interaction (influence of the green beard on the expression of the altruistic trait), as well as the costs and benefits of the altruistic behavior. We further show that this correlation does not necessarily have to be high and support our analytical results by simulations.

Abstract Maternal effects are prevalent in nature and significantly contribute to variation in phenotypic trait expression. However, little attention has been paid to the factors shaping variation in the traits mediating these effects (maternal effectors). Specific maternal effectors are often not identified, and typically they are assumed to be inherited in an additive genetic and autosomal manner. Given that these effectors can cause long‐lasting effects on offspring phenotype, it is likely that they may also affect themselves in the next generation. Although the existence of such cascading maternal effects has been discussed and modeled, empirical examples of such effects are rare, let alone quantitative estimates of their strength and evolutionary consequences. Here, we demonstrate that the investment a mother makes in her eggs positively affects the egg investment of her daughters. Through reciprocally crossing artificially selected lines for divergent prenatal maternal investment in Japanese quail (Coturnix japonica), we demonstrate that the size of eggs daughters lay resembles the egg size of their maternal line significantly more than that of their paternal line, highlighting that egg size is in part maternally inherited. Correspondingly, we find that variation in the daughters' egg size is in part determined by maternal identity, in addition to substantial additive genetic effects. Furthermore, this maternal variance in offspring egg size is fully explained by maternal egg size, demonstrating the presence of a positive cascading effect of maternal egg size on offspring egg size. Finally, we use an evolutionary model to quantify the consequences of covariance between cascading maternal and additive genetic effects for both maternal effector and offspring body mass evolution. Our study demonstrates that by amplifying the amount of variation available for selection to act on, positive cascading maternal effects can significantly enhance the evolutionary potential of maternal effectors and the offspring traits that they affect.

Objective Sow longevity is important for efficient and profitable pig farming. Recently, there has been an increasing interest in social genetic effect (SGE) of pigs on stress-tolerance and behavior. The present study aimed to estimate genetic correlations among average daily gain (ADG), stayability (STAY), and number of piglets born alive at the first parity (NBA1) in Korean Yorkshire pigs, using a model including SGE. Methods The phenotypic records of ADG and reproductive traits of 33,120 and 11,654 pigs, respectively, were evaluated. The variances and (co) variances of the studied traits were estimated by a multi-trait animal model applying the Bayesian with linear-threshold models using Gibbs sampling. Results The direct and SGEs on ADG had a significantly negative (−0.30) and neutral (0.04) genetic relationship with STAY, respectively. In addition, the genetic correlation between the social effects on ADG and NBA1 tended to be positive (0.27), unlike the direct effects (−0.04). The genetic correlation of the total effect on ADG with that of STAY was negative (−0.23) but non-significant, owing to the social effect. Conclusion These results suggested that total genetic effect on growth in the SGE model might reduce the negative effect on sow longevity because of the growth potential of pigs. We recommend including social effects as selection criteria in breeding programs to obtain satisfactory genetic changes in both growth and longevity.

Queens of eusocial species live extraordinarily long compared to their workers. So far, it has been argued that these lifespan divergences are readily explained by the classical evolutionary theory of ageing. As workers predominantly perform risky tasks, such as foraging and nest defense, and queens stay in the well‐protected nests, selection against harmful genetic mutations expressed in old age should be weaker in workers than in queens due to caste differences in extrinsic mortality risk, and thus, lead to the evolution of longer queen and shorter worker lifespans. However, these arguments have not been supported by formal models. Here, we present a model for the evolution of caste‐specific ageing in social insects, based on Williams' antagonistic pleiotropy theory of ageing. In individual‐based simulations, we assume that mutations with antagonistic fitness effects can act within castes, that is, mutations in early life are accompanied by an antagonistic effect acting in later life, or between castes, where antagonistic effects emerge due to caste antagonism or indirect genetic effects between castes. In monogynous social insect species with sterile workers, large lifespan divergences between castes evolved under all different scenarios of antagonistic effects, but regardless of the degree of caste‐specific extrinsic mortality. Mutations with antagonistic fitness effects within castes reduced lifespans of both castes, while mutations with between‐caste antagonistic effects decreased worker lifespans more than queen lifespans, and consequently increased lifespan divergences. Our results challenge the central explanatory role of extrinsic mortality for caste‐specific ageing in eusocial organisms and suggest that antagonistic pleiotropy affects castes differently due to reproductive monopolization by queens, hence, reproductive division of labor. Finally, these findings provide new insights into the evolution of tissue‐specific ageing in multicellular organisms in general. [ABSTRACT FROM AUTHOR]

Indirect genetic effects from relatives may result in misleading quantifications of heritability, but can also be of interest in their own right. In this paper we propose Trio-GCTA, a model for separating direct and indirect genetic effects when genome-wide single nucleotide polymorphism data have been collected from parent-offspring trios. The model is applicable to phenotypes obtained from any of the family members. We discuss appropriate parameter interpretations and apply the method to three exemplar phenotypes: offspring birth weight, maternal relationship satisfaction, and paternal body-mass index, using real data from the Norwegian Mother, Father and Child Cohort Study (MoBa). [ABSTRACT FROM AUTHOR]

We investigate the evolution of a gene for paternal care, with pleiotropic effects on male mating fitness and offspring viability, with and without extrapair copulations (EPCs). We develop a population genetic model to examine how pleiotropic effects of a male mating advantage and paternal care are affected by "good genes" and EPCs. Using this approach, we show that the relative effects of each on fitness do not always predict the evolutionary change. We then find the line of combinations of mating success and paternal care that bisects the plane of possible values into regions of positive or negative gene frequency change. This line shifts when either good genes or EPCs are introduced, thereby expanding or contracting the region of positive gene frequency change and significantly affecting the evolution of paternal care. Predictably, a direct viability effect of "good genes" that enhances offspring viability constrains or expands the parameter space over which paternal care can evolve, depending on whether the viability effect is associated with the paternal care allele or not. In either case, the effect of a "good gene" that enhances offspring viability is substantial; when strong enough, it can even facilitate the evolution of poor paternal care, where males harm their young. When nonrandom mating is followed by random EPCs, the genetic regression between sire and offspring is reduced and, consequently, the relative strengths of selection are skewed away from paternal care and toward the male mating advantage. However, when random mating is followed by nonrandom EPCs, a situation called "trading up" by females, we show that selection is skewed in the opposite direction, away from male mating advantage and toward paternal care across the natural range of EPC frequencies. [ABSTRACT FROM AUTHOR]

For understanding how social behaviour evolves and responds to selection, we need to be able to accurately estimate heritability with quantitative genetic models. More recently, this has moved into using node‐specific statistics from social networks as social phenotypes. However, parameter estimation can be problematic because social phenotypes are not independent observations and standard models tend to ignore the uncertainties around their estimates.Here I present a framework using latent variable modelling to account for these dependencies and uncertainties. I use edge weights, rather than node‐specific network statistics, as dependent variables. From these edge weights, two types of latent (i.e. unobserved) phenotypes are estimated: the individual tendency to be social (i.e. social tendency) and the relative contribution to associations (i.e. social governance). Effects of the social environment and indirect genetic effects are accounted for in the model and can be estimated post hoc. If edge weights are a proportion (e.g. simple ratio index) their uncertainty can be accounted for by a binomial sampling process.I illustrate this method in Stan, a flexible Bayesian inference library, using a publicly available dataset on bottlenose dolphin networks. This method not only accounts for dependencies and uncertainties, it also illuminates aspects of social evolution which are not observed with standard quantitative genetic models. For instance, indirect genetic effects models predict heritable variation in sociality (21.9%), while latent variable modelling shows heritability of social tendency (28.7%), but not for social governance (0.0%). Covariates at different levels in the model (edge and node level) highlight differences in sociality between different foraging strategies and the sexes.This example shows that not properly accounting for the assumptions underlying the use of social network statistics can have misleading effects on conclusions. Although some model assumption violations are less common, others are inherit to the study of (semi)wild populations. The presented framework offers solutions for some critical assumptions and is a flexible tool to further develop and tailor to the needs of specific studies, to ensure the proper fit to the study system. [ABSTRACT FROM AUTHOR]

We investigated indirect genetic effects (IGEs), also known as genetic nurture, in education with a novel approach that uses phased data to include parent-offspring pairs in the transmitted/nontransmitted study design. This method increases the power to detect IGEs, enhances the generalizability of the findings, and allows for the study of effects by parent-of-origin. We validated and applied this method in a family-based subsample of adolescents and adults from the Lifelines Cohort Study in the Netherlands (N = 6147), using the latest genome-wide association study data on educational attainment to construct polygenic scores (PGS). Our results indicated that IGEs play a role in education outcomes in the Netherlands: we found significant associations of the nontransmitted PGS with secondary school level in youth between 13 and 24 years old as well as with education attainment and years of education in adults over 25 years old (β = 0.14, 0.17 and 0.26, respectively), with tentative evidence for larger maternal IGEs. In conclusion, we replicated previous findings and showed that including parent-offspring pairs in addition to trios in the transmitted/nontransmitted design can benefit future studies of parental IGEs in a wide range of outcomes., (© 2024 The Authors. Genetic Epidemiology published by Wiley Periodicals LLC.)

Oxytocin-like peptides have been implicated in the regulation of a wide range of social behaviors across taxa. On the other hand, the social environment, which is composed of conspecifics that may vary in their genotypes, also influences social behavior, creating the possibility for indirect genetic effects. Here, we used a zebrafish oxytocin receptor knockout line to investigate how the genotypic composition of the social environment (Gs) interacts with the oxytocin genotype of the focal individual (Gi) in the regulation of its social behavior. For this purpose, we have raised wild-type or knock-out zebrafish in either wild-type or knock-out shoals and tested different components of social behavior in adults. GixGs effects were detected in some behaviors, highlighting the need to control for GixGs effects when interpreting results of experiments using genetically modified animals, since the genotypic composition of the social environment can either rescue or promote phenotypes associated with specific genes.

Mutant zebrafish exhibit different behaviours depending on the genetic background of the fish they were raised with.