Ethical debates around genetic enhancement tend to include an argument that the technology will eventually be fairly accessible once available. That we can fairly distribute genetic enhancement has become a moral defence of genetic enhancement. Two distribution solutions are argued for, the first being equal distribution. Equality of access is generally believed to be the fairest and most just method of distribution. Second, equitable distribution: providing genetic enhancements to reduce social inequalities. In this paper, I make two claims. I first (...) argue that the very assumption that genetic enhancements can be distributed fairly is problematic when considering our understanding of gene–environment interactions, for example, epigenetics. I then argue that arguments that genetic enhancements are permissible because the intended benefits can be distributed fairly as intended are misinformed. My first claim rests on the assertion that genetic enhancements do not enhance traits in a vacuum; genes are dependent on conducive environments for expression. If society cannot guarantee fair environments, then any benefit conferred from being genetically enhanced will be undermined. Thus, any argument that the distribution of genetic enhancements will be fair and that the technology is therefore morally permissible, is mistaken. (shrink)

Although the field of psychiatry has witnessed the proliferation of studies on Gene x Environment (GxE) interactions, still limited is the knowledge we possess of GxE interactions regarding developmental disorders. In this perspective paper, we discuss why GxE interaction studies are needed to broaden our knowledge of developmental disorders. We also discuss the different roles of hazardous versus self-generated environmental factors and how these types of factors may differentially engage with an individual’s genetic background in predicting a (...) resulting phenotype. Then, we present exemplar studies that highlight the role of GxE in predicting atypical developmental trajectories as well as provide insight regarding treatment outcomes. Supported by these examples, we explicate the need to move beyond merely examining statistical interactions between genes and the environment, and to investigate specific genetic susceptibility and environmental contexts that drive developmental disorders. We propose that further parsing of genetic and environmental components is required to fully understand the unique contribution of each factor to the etiology of developmental disorders. Finally, with a greater appreciation of the complexities of GxE interaction, this discussion will converge upon the potential implications for clinical and translational research. (shrink)

The presence of gene–environment statistical interaction and correlation in biological development has led both practitioners and philosophers of science to question the legitimacy of heritability estimates. The paper offers a novel approach to assess the impact of GxE and rGE on the way genetic and environmental causation can be partitioned. A probabilistic framework is developed, based on a quantitative genetic model that incorporates GxE and rGE, offering a rigorous way of interpreting heritability estimates. Specifically, given an estimate (...) of heritability and the variance components associated with estimates of GxE and rGE, I arrive at a probabilistic account of the relative effect of genes and environment. (shrink)

Scientists now agree that common diseases arise through interactions of genetic and environmental factors, but there is less agreement about how scientific research should account for these interactions. This paper examines the politics of quantification in gene–environment interaction research. Drawing on interviews and observations with GEI researchers who study common, complex diseases, we describe quantification as an unfolding moral economy of science, in which researchers collectively enact competing “virtues.” Dominant virtues include molecular precision, in which behavioral and (...) social risk factors are moved into the body, and “harmonization,” in which scientists create large data sets and common interests in multisited consortia. We describe the negotiations and trade-offs scientists enact in order to produce credible knowledge and the forms of discipline that shape researchers, their practices, and objects of study. We describe how prevailing techniques of quantification are premised on the shrinking of the environment in the interest of producing harmonized data and harmonious scientists, leading some scientists to argue that social, economic, and political influences on disease patterns are sidelined in postgenomic research. We consider how a variety of GEI researchers navigate quantification’s productive and limiting effects on the science of etiological complexity. (shrink)

I provide a history of research on G×E in this article, showing that there have actually been two distinct concepts of G×E since the very origins of this research. R. A. Fisher introduced what I call the biometric concept of G×E, or G×EB, while Lancelot Hogben introduced what I call the developmental concept of G×E, or G×ED. Much of the subsequent history of research on G×E has largely consisted in the separate legacies of these separate concepts, along with the (sometimes (...) acrimonious) disputes that have arisen time and again when employers of each have argued over the appropriate way to conceptualize the phenomenon. With this history in place, I then consider more recent attempts to distinguish between different concepts of G×E, paying particular attention to the commonly made distinction between “statistical interaction” and “interactionism,” and also Michael Rutter’s distinction between “statistical interaction” and “the biological concept of interaction.” I argue that the history of the separate legacies of G×EB and G×ED better supports Rutter’s analysis of the situation, and that this analysis best paves the way for an integrative relationship between the various scientists investigating the place of G×E in the etiology of complex traits. (shrink)

In a widely acclaimed study from 2002, researchers found a case of gene-environment interaction for a gene controlling neuroenzymatic activity (low vs. high), exposure to childhood maltreatment, and antisocial personality disorder (ASPD). Cases of gene-environment interaction are generally characterized as evincing a genetic predisposition; for example, individuals with low neuroenzymatic activity are generally characterized as having a genetic predisposition to ASPD. I first argue that the concept of a genetic predisposition fundamentally misconstrues these (...) cases of gene-environment interaction. This misconstrual will be diagnosed, and then a new concept—interactive predisposition—will be introduced. I then show how this conceptual shift reconfigures old questions and raises new questions for genetic screening. Attempts to screen embryos or fetuses for the gene associated with low neuroenzymatic activity with an eye towards selecting against the low-activity variant fall prey to the myth of pre-environmental prediction; attempts to screen newborns for the gene associated with low neuroenzymatic activity with an eye towards early intervention will have to face the interventionist’s dilemma. (shrink)

In our commentary we ask whether we should ultimately endeavour to find the deep causes of behaviours? Then we discuss two extensions of the proposed framework: (1) Mendelian randomisation and (2) hypothesis-free gene–environment interaction (leveraging heterogeneity in genetic associations). These complementary methods help move us towards second-generation causal knowledge, ultimately understanding mechanistic pathways and identifying more effective intervention targets.

The target article approaches individual differences in terms of phenotypic differences developing through the interaction between a specific genetic make up and environmental variables. This interaction is proposed to be cooperative and oriented toward a progressive stabilisation of the trait. However, experimental data from animal studies indicate that environmental pressure promotes dramatic changes in phenotypic expression in mature organisms. Indeed, environmental constraint not only promotes the phenotypic expression of facilitated VTA-NAS DA transmission in genotype-resistant individuals; it also inhibits (...) its expression in genetically prone individuals. This is in line with negative genotype-environment correlation revealed by behavior genetics. (shrink)

Extensive research has demonstrated that rs1360780, a common single nucleotide polymorphism within the FKBP5 gene, interacts with early-life stress in predicting psychopathology. Previous results suggest that carriers of the TT genotype of rs1360780 who were exposed to child abuse show differences in structure and functional activation of emotion-processing brain areas belonging to the salience network. Extending these findings on intermediate phenotypes of psychopathology, we examined if the interaction between rs1360780 and child abuse predicts resting-state functional connectivity (rsFC) between (...) the amygdala and other areas of the salience network. We analyzed data of young European adults from the general population (N = 774; mean age = 18.76 years) who took part in the IMAGEN study. In the absence of main effects of genotype and abuse, a significant interaction effect was observed for rsFC between the right centromedial amygdala and right posterior insula (p <.025, FWE-corrected), which was driven by stronger rsFC in TT allele carriers with a history of abuse. Our results suggest that the TT genotype of rs1360780 may render individuals with a history of abuse more vulnerable to functional changes in communication between brain areas processing emotions and bodily sensations, which could underlie or increase the risk for psychopathology. (shrink)

The main public health advantages of examining gene by environment interactions in externalizing behavior lie in the realm of personalized interventions. Nevertheless, the incorporation of genetic data in randomized controlled trials is fraught with difficulties and raises ethical questions. This paper has been written from the perspective of developmental psychologists who, as researchers, see themselves confronted with important and in part new kinds of ethical questions arising from G × E research in social sciences. The aim is to (...) explicate and discuss ethical questions, based on the conviction that what is ethically salient in a research setting will also be relevant in that area of public healthcare incorporating research findings. The ethical questions discussed include: whether it is ethically responsible to withhold an effective treatment; to what extent genetic results should be disclosed; whether researchers should be allowed to collect genetic data of both child and parent; and what are costs and benefits of personalized interventions based on screening. We made an attempt to address these questions, but it is up to researchers to determine whether the solutions are suitable for their G × E research in social sciences. (shrink)

Behavioural phenotypes have been explained by genetic and environmental factors (E) and their interaction. Here we suggest a rethinking of the E factor. Passively incurred environmental influences (E pass) and actively copied information and behaviour (E act) may be distinguished at shared and non-shared level. We argue that E act underlies mutation and selection and is the base of gene-independent heritability.

In this essay we consider some of the characteristics of adaptive biological systems and how these might work as models in designing a robot intended for the exploration of complex environments. Trying to design a robot that has such properties forces one to think hard about the nature of those properties. Here we have one intersection between philosophy and computing. We consider the nature of adaptability and some properties of complex biological systems that are relevant to designing adaptive robots, including (...) direct perception, animacy, affordances, redundant degress of freedom, collective decisions, and emergent properties. We explain how these concepts were used in the development of a robotic arm. (shrink)

This paper's aim is threefold. First, I wish to show that there is an analogy in section nine that arises out of the interaction of the interlocutors; this analogy is, or has, a certain comic adequatic to the traditional (e.g. Aquinas's) arguments about proofs for the existence of God. Second, Philo's seemingly inconsequential example of the strange necessity of products of 9 in section nine is a perfected analogy of the broken arguments actually given in that section, destroying Philo's (...) earlier arguments. Finally, I raise the question of the designer's intent in creating such a humourous piece. (shrink)

This paper's aim is threefold. First, I wish to show that there is an analogy in section nine that arises out of the interaction of the interlocutors; this analogy is, or has, a certain comic adequatic to the traditional arguments about proofs for the existence of God. Second, Philo's seemingly inconsequential example of the strange necessity of products of 9 in section nine is a perfected analogy of the broken arguments actually given in that section, destroying Philo's earlier arguments. (...) Finally, I raise the question of the designer's intent in creating such a humourous piece. (shrink)

Plato’s dialogues are self-defined as works of mimetic art, and the ancients clearly consider mimesis as working naturally before reason and beneath it. Such aview connects with two contemporary ideas—Rene Girard’s idea of the mimetic basis of culture and neurophysiological research into mirror neurons. Individualityarises out of, and can collapse back into our mimetic origin. This para-rational notion of mimesis as that in which and by which all our knowledge is framed requires we not only concern ourselves with Socrates’s arguments (...) and distinctions, but also see how the dramatic interaction of the characters is working (or not) on/in the characters, and consider how watching the interaction, hearing the parables and myths, and thinking through the arguments and interactions is meant to effect us. That Plato creates mimeses means he aims at passional conversion not merely argumentative worth, since mimesis aims to (and does) work on the passions. (shrink)

This article describes and reflects upon Australia's extensive, federally-mandated, environmental education program. This program is based on a National Conservation Strategy which went into effect in 1989. But the program has massive support on the state and local levels as well. In addition to traditional classroom study of the environment and environmental issues, Audtralian Students do composting, re-vegetation of local canyons, and other hands-on activities. In many areas of the students' deatiledreports become the data base for the government's environmental (...) monitoring program. A remarkable aspect of environmental education in Australia is the web of groups and individuals who are involved: local farmers, Aboriginal peoples, banks, local nurseries, and all levels of government, along with environmental organizations like Greening Astraila and Landcare.In contrast to Australia, the United States lacks a systematic educational program focused on the environment. The article concludes by summarizing the strengths of the Australian program and criticizing the American failure to establish such a program. Reasons for this failure are suggested. Finally, a general contrast is offered, showing the differences between two philosophies of education—the Technocratic Philosophy of Education vs. the Holistic Philosophy of Education. (shrink)

In the multidisciplinary field of developmental cognitive neuroscience, statistical associations between levels of description play an increasingly important role. One example of such associations is the observation of correlations between relatively common gene variants and individual differences in behavior. It is perhaps surprising that such associations can be detected despite the remoteness of these levels of description, and the fact that behavior is the outcome of an extended developmental process involving interaction of the whole organism with a variable (...) environment. Given that they have been detected, how do such associations inform cognitive-level theories? To investigate this question, we employed a multiscale computational model of development, using a sample domain drawn from the field of language acquisition. The model comprised an artificial neural network model of past-tense acquisition trained using the backpropagation learning algorithm, extended to incorporate population modeling and genetic algorithms. It included five levels of description—four internal: genetic, network, neurocomputation, behavior; and one external: environment. Since the mechanistic assumptions of the model were known and its operation was relatively transparent, we could evaluate whether cross-level associations gave an accurate picture of causal processes. We established that associations could be detected between artificial genes and behavioral variation, even under polygenic assumptions of a many-to-one relationship between genes and neurocomputational parameters, and when an experience-dependent developmental process interceded between the action of genes and the emergence of behavior. We evaluated these associations with respect to their specificity, to their developmental stability, and to their replicability, as well as considering issues of missing heritability and gene–environment interactions. We argue that gene–behavior associations can inform cognitive theory with respect to effect size, specificity, and timing. The model demonstrates a means by which researchers can undertake multiscale modeling with respect to cognition and develop highly specific and complex hypotheses across multiple levels of description. (shrink)

Quantitative genetics (QG) analyses variation in traits of humans, other animals, or plants in ways that take account of the genealogical relatedness of the individuals whose traits are observed. “Classical” QG, where the analysis of variation does not involve data on measurable genetic or environmental entities or factors, is reformulated in this article using models that are free of hypothetical, idealized versions of such factors, while still allowing for defined degrees of relatedness among kinds of individuals or “varieties.” The (...) class='Hi'>gene - free formulation encompasses situations encountered in human QG as well as in agricultural QG. This formulation is used to describe three standard assumptions involved in classical QG and provide plausible alternatives. Several concerns about the partitioning of trait variation into components and its interpretation, most of which have a long history of debate, are discussed in light of the gene-free formulation and alternative assumptions. That discussion is at a theoretical level, not dependent on empirical data in any particular situation. Additional lines of work to put the gene-free formulation and alternative assumptions into practice and to assess their empirical consequences are noted, but lie beyond the scope of this article. The three standard QG assumptions examined are: (1) partitioning of trait variation into components requires models of hypothetical, idealized genes with simple Mendelian inheritance and direct contributions to the trait; (2) all other things being equal, similarity in traits for relatives is proportional to the fraction shared by the relatives of all the genes that vary in the population (e.g., fraternal or dizygotic twins share half of the variable genes that identical or monozygotic twins share); (3) in analyses of human data, genotype-environment interaction variance (in the classical QG sense) can be discounted. The concerns about the partitioning of trait variation discussed include: the distinction between traits and underlying measurable factors; the possible heterogeneity in factors underlying the development of a trait; the kinds of data needed to estimate key empirical parameters; and interpretations based on contributions of hypothetical genes; as well as, in human studies, the labeling of residual variance as a non-shared environmental effect; and the importance of estimating interaction variance. (shrink)

On some occasions of self-reference there can be two equally viable forms available to speakers: individual self-reference and collective self-reference. This means that selection of one or the other in talk-in-interaction can — akin to the selection of terms for reference to non-present persons — be guided by such considerations as recipient design and action formation. As a strategy for investigating the selection of self-reference terms, this article examines repairs to self-reference that change the form of reference from individual (...) to collective and vice versa. We first identify two repair operations found in the domain of self-reference: aggregation and extraction and then we track the use of both operations across a range of positions in the repair initiation opportunity space. Finally we consider some of the interactional uses of aggregation and extraction repairs in resolving sources of troubles associated with speaker epistemic authority and responsibility for described actions. (shrink)

Although biologists and philosophers of science generally agree that genes cannot determine the forms of biological and psychological traits, students, journalists, politicians, and other members of the general public nonetheless continue to embrace genetic determinism. This article identifies some of the concerns typically raised by individuals when they first encounter the systems perspective that biologists and philosophers of science now favor over genetic determinism, and uses arguments informed by that perspective to address those concerns. No definitive statements can yet be (...) made about why genetic determinism has proven so resilient in the face of empirical evidence pointing up its deficiencies, but conveying the essential interdependence of 'nature' and 'nurture' to the general public will likely require deployment of the arguments that systems theorists ordinarily use to reject genetic determinism. In addition, the elaboration of new metaphors that focus attention on the dynamic nature of trait construction will likely prove valuable, because re-conceptualizing notions like 'genes' and 'nature' will probably be one of the most effective ways to help students and the general public abandon the genetic determinism that biologists now recognize as indefensible. (shrink)

Throughout evolution, there has been interaction and exchange between RNA pools in the environment, and DNA and RNA pools of eukaryotic organisms. Metagenomic and metatranscriptomic sequencing of invertebrate hosts and their microbiota has revealed a rich evolutionary history of RNA virus shuttling between species. Horizontal transfer adapted the RNA pool for successful future interactions which lead to zoonotic transmission and detrimental RNA viral pandemics like SARS‐CoV2. In eukaryotes, noncoding RNA (ncRNA) is an established mechanism derived from prokaryotes to (...) defend against viral attack through innate immunity and regulation of host‐derived mRNA. Transgenerational inheritance of ncRNA is evidence for feedforward adaptive immunity and epigenetically encoded environmental change across generations, which may explain the ‘‘missing heritability’’ of common disease. Causal graph theory and the Price Equation can model epigenetic inheritance involving dynamic internal and external RNA pools. Experimental designs should include metatranscriptomic analyses to understand how ncRNA responds to rapidly changing environmental conditions, within and between organisms, and across generations. (shrink)

A discussion of plasticity genes and the genetic architecture of gene-environment interactions.

Many cases of gene‐environment interaction, or , are misconstrued as evincing a genetic predisposition. I diagnose this misconstrual and then introduce a new concept— interactive predisposition —to correct for the mistake. I conclude by examining how recent debates over screening for individual predispositions are related to older debates about group differences between populations , drawing on the lessons of the latter to inform the former. †To contact the author, please write to: Department of Philosophy, University of Utah, (...) Salt Lake City, UT 84112; e‐mail: [email protected]. (shrink)

Accumulating research has identified the interactive effects of catechol-O-methyltransferase gene Val158Met polymorphism and environmental factors on aggression. However, available evidence was mainly based upon correlational design, which yields mixed findings concerning who are more affected by environmental conditions and has been challenged for the low power of analyses on gene–environment interaction. Drawing on a mixed design, we scrutinized how COMT Val158Met polymorphism impacts on aggression, assessed by hostility, aggressive motivation, and aggressive behavior, under different social conditions (...) in a sample of 70 Chinese male undergraduate students. We found that both Val/Val homozygote and Met alleles carriers showed differences in the feelings of hostility and aggressive motivation under conditions of exclusion versus inclusion, but these differences were more pronounced for Met allele carriers. These findings implied that COMT Val158Met polymorphism did not respond to environmental stimuli in an all-or-none way and shed light on the importance of examining the gene–environment interaction using a mixed design. (shrink)

Genetics is in a postgenomic era, and this article illustrates this epistemological evolution using the debate between developmental criticism and traditional biometric genetics about gene × environment interaction. Quantitative geneticists are blamed for failing to respect the complexity of development; as a response, they claim a defensive position, called isolationist pluralism, which supports the idea that studying development is not their problem. But postgenomics seems to have accepted and integrated some developmental criticisms and the isolationist perspective has (...) been challenged during the last few years. The developmental and quantitative traditions actually represent two different levels of analysis, but biometrics has also a clear developmental explanatory potential as it suggests statistically the existence of mechanical causes. Both traditions work together to go ever further in the knowledge of the phenomena being studied. Postgenomic pluralism, instead of being isolationist, may be considered pragmatic. (shrink)

The discursive explosion that was provoked by the new genetics could support the impression that the ethical and social problems posed by the new genetics are somehow exceptional in their very nature. According to this view we are faced with special ethical and social problems that create a challenge so fundamental that the special label of genethics is needless to justify. The historical account regarding the evolution of the gene concepts could serve us to highlight the limits of what (...) we know about genes and what we can do with genes. The widespread notion about the exceptionality of genetic knowledge and its applicative possibilities is hardly justifiable and leads to misunderstandings regarding the conceptualization of the ethical and social problems we might face. Following a more realistic interpretation of the role of genes in human life we might avoid a whole set of fictive dilemmas and counterproductive regulatory efforts in bioethics. Bioethical discourse should move from the gene-centered scientific discourse toward the more sophisticated and complex discourses where human development represented as a matter of complex interactions between genomes and environments, between genes, educational factors, nutritional regimes, and other different developmental resources. If a gene is seen as one among the different developmental resources that are shaping a given human trait then both genethics and genetic exceptionalism could hardly be represented as a justified approach in discussing the ethical and social problems of genetics. (shrink)

People respond to metaphors as much with regard to the emotions that they generate as to their referential, comparative contents. Interviews with non-geneticists about preferred metaphors for gene-environment interaction that illustrate this tendency are reported. These interviews also reveal the dynamic tendency of such emotional responses. A second set of interviews shows that lay people may preferentially use a metaphor of "virus" or "disease" for talking about genes, as opposed to the coding metaphors transmitted through the mass (...) media and reportedly preferred by geneticists. An explanation based on the differently situated emotions of these groups is proposed. It is proposed that the prominence of emotions in responding to genetics indicates the importance of incorporating analyses of emotions instead of simple principles into policy formulation about genetics. (shrink)

Social institutions are the laws, informal rules, and conventions that give durable structure to social interactions within a population. Such institutions are typically not designed consciously, are heritable at the population level, are frequently but not always group benefi cial, and are often symbolically marked. Conceptualizing social institutions as one of multiple possible stable cultural equilibrium allows a straightforward explanation of their properties. The evolution of institutions is partly driven by both the deliberate and intuitive decisions of individuals and collectivities. (...) The innate components of human psychology coevolved in response to a culturally evolved, institutional environment and refl ect a prosocial tendency of choices we make about institutional forms. (shrink)

What are genes? What do genes do? These seemingly simple questions are in fact challenging to answer accurately. As a result, there are widespread misunderstandings and over-simplistic answers, which lead to common conceptions widely portrayed in the media, such as the existence of a gene 'for' a particular characteristic or disease. In reality, the DNA we inherit interacts continuously with the environment and functions differently as we age. What our parents hand down to us is just the beginning (...) of our life story. This comprehensive book analyses and explains the gene concept, combining philosophical, historical, psychological and educational perspectives with current research in genetics and genomics. It summarises what we currently know and do not know about genes and the potential impact of genetics on all our lives. Making Sense of Genes is an accessible but rigorous introduction to contemporary genetics concepts for non-experts, undergraduate students, teachers and healthcare professionals. (shrink)

This essay considers biotrophic cyst and root‐knot nematodes in relation to their biology, host–parasite interactions and molecular genetics. These nematodes have to face the biological consequences of the physical constraints imposed by the soil environment in which they live while their hosts inhabit both above and below ground environments. The two groups of nematodes appear to have adopted radically different solutions to these problems with the result that one group is a host specialist and reproduces sexually while the other (...) has an enormous host range and reproduces by mitotic parthenogenesis. We consider what is known about the modes of parasitism used by these nematodes and how it relates to their host range, including the surprising finding that parasitism genes in both nematode groups have been recruited from bacteria. The nuclear and mitochondrial genomes of these two nematode groups are very different and we consider how these findings relate to the biology of the organisms. BioEssays 30:249–259, 2008. © 2008 Wiley Periodicals, Inc. (shrink)

The ArgumentThis article considers three major problems with the concept of genes for human personality traits: uncertainty about what human personality is; what we mean when we say there is a gene “for” a mental attribute; and the complexity of interactions between genes and environment, and among the genes themselves. It then draws on examples from empirical human genetic studies by the author and his colleagues in order to suggest that the concept of genes for human personality traits (...) nevertheless does have some validity, and also that we may be on the brink of discovering genes with major effects on human personality. This possibility, in particular its ethical aspects, has aroused some public concern. It is suggested that confidential information about an individual's genes does not differ in principle from other confidential information about him or her, and that the ability to affect genes and their expression, temporarily or permanently, does not differ ethically from our current ability to affect other aspects of an individual's physical and psychological functioning. Genes for potential offspring, contained in ova and sperm cells, constitute a special case. (shrink)

Behavioral genetics and cultural evolution have both revolutionized our understanding of human behavior – largely independent of each other. Here, we reconcile these two fields under a dual inheritance framework, offering a more nuanced understanding of the interaction between genes and culture. Going beyond typical analyses of gene–environment interactions, we describe the cultural dynamics that shape these interactions by shaping the environment and population structure. A cultural evolutionary approach can explain, for example, how factors such as (...) rates of innovation and diffusion, density of cultural subgroups, and tolerance for behavioral diversity impact heritability estimates, thus yielding predictions for different social contexts. Moreover, when cumulative culture functionally overlaps with genes, genetic effects become masked, unmasked, or even reversed, and the causal effects of an identified gene become confounded with features of the cultural environment. The manner of confounding is specific to a particular society at a particular time, but a WEIRD (western, educated, industrialized, rich, and democratic) sampling problem obscures this boundedness. Cultural evolutionary dynamics are typically missing from models of gene-to-phenotype causality, hindering generalizability of genetic effects across societies and across time. We lay out a reconciled framework and use it to predict the ways in which heritability should differ between societies, between socioeconomic levels, and other groupings within some societies but not others, and over the life course. An integrated cultural evolutionary behavioral genetic approach cuts through the nature–nurture debate and helps resolve controversies in topics such as IQ. (shrink)

The interactions between genetic and environmental risk factors contribute to the aetiology of complex human diseases. Genome‐wide association studies (GWAS) have revealed that most of the genetic variants associated with complex diseases are located in the non‐coding part of the genome, preferentially within enhancers. Enhancers are distal cis‐regulatory elements composed of clusters of transcription factors binding sites that positively regulate the expression of their target genes. The generation of genome‐wide maps for histone marks (e.g., H3K27ac), chromatin accessibility and transcription factor (...) and coactivator (e.g., p300) binding profiles have enabled the identification of enhancers across many human cell types and tissues. Nonetheless, the functional and pathological consequences of the majority of disease‐associated genetic variants located within enhancers seem to be rather minor under normal conditions, thus questioning their medical relevance. Here we propose that, due to the prevalence of enhancer redundancy, the pathological effects of many disease‐associated non‐coding genetic variants might be preferentially (or even only) manifested under environmental stress. (shrink)

The evolutionary implications of environmental change due to organismic action remain a controversial issue, after a decades—long debate on the subject. Much of this debate has been conducted in qualitative fashion, despite the availability of mathematical models for organism–environment interactions, and for gene frequencies when allele fitness can be related to exploitation of a particular environmental resource. In this article we focus on representative models dealing with niche construction, ecosystem engineering, the Gaia Hypothesis and community interactions of Lotka–Volterra (...) type, and show that their quantitative character helps bring into sharper focus the similarities and differences among their respective theoretical contexts. (shrink)

In Italy, a judge reduced the sentence of a defendant by 1 year in response to evidence for a genetic predisposition to violence. The best characterized of these genetic differences, those in the monoamine oxidase A (MAOA), were cited as especially relevant. Several months previously in the USA, MAOA data contributed to a jury reducing charges from 1st degree murder (a capital offence) to voluntary manslaughter. Is there a rational basis for this type of use of MAOA evidence in criminal (...) court? This paper will review in context recent work on the MAOA gene–environment interaction in predisposing individuals to violence and address the relevance of such findings to murder trials. Interestingly, the MAOA genetic variants impact future violence and aggression only when combined with the adverse environmental stimuli of childhood maltreatment. Thus nature and nurture interact to determine the individual’s risk. Based on current evidence, I argue there is a weak case for mitigation. But should future experiments confirm the hypothesis that individual differences in impulse control and response to provocation found in MAOA-L men (without abuse) are significantly magnified when combined with childhood maltreatment, the case could turn into a stronger one. (shrink)

The vast majority (> 95%) of single-gene mutations in yeast affect not only the expression of the mutant gene, but also the expression of many other genes. These data suggest the presence of a previously uncharacterized ‘gene expression network’—a set of interactions between genes which dictate gene expression in the native cell environment. Here, we quantitatively analyze the gene expression network revealed by microarray expression data from 273 different yeast gene deletion mutants.(1) We (...) find that gene expression interactions form a robust, error-tolerant ‘scale-free’ network, similar to metabolic pathways(2) and artificial networks such as power grids and the internet.(3-5) Because the connectivity between genes in the gene expression network is unevenly distributed, a scale-free organization helps make organisms resistant to the deleterious effects of mutation, and is thus highly adaptive. The existence of a gene expression network poses practical considerations for the study of gene function, since most mutant phenotypes are the result of changes in the expression of many genes. Using principles of scale-free network topology, we propose that fragmenting the gene expression network via ‘genome-engineering’ may be a viable and practical approach to isolating gene function. BioEssays 24:267–274, 2002. © 2002 Wiley Periodicals, Inc.; DOI 10.1002/bies.10054. (shrink)

This paper examines the changing meanings of the concept of 'biology', and of its opposition to 'culture', through an analysis of the ways in which anthropologists have sought to refute the idea that humanity is divided into distinct races. Efforts to redefine all extant humans as belonging to a single sub-species, or to replace 'race' with 'culture', only serve to perpetuate raciological thinking. This kind of thinking had its origins in the moral evaluation of physical difference, the construction of hierarchy (...) and essentialist typology. In its 1996 'Statement on Race', the American Association of Physical Anthropologists ruled out any connection between the biological and cultural characteristics of human beings. Yet the statement is internally inconsistent in the meanings it attributes to both biology and culture. These shifts in meaning correspond to phases in the history of anthropology, identified here as the Enlightenment phase (culture as a process of civilisation drawing on universal biopsychological capacities), the Consensual phase (culture as diverse traditions inscribed upon a common biological substrate) and the Interactionist phase (behaviour as the product of an interaction between culturally and genetically transmitted information in a given environment). The paper seeks an alternative, relational approach that focuses on the dynamics of developmental systems. Only through such an approach, it is argued, can we wrest biology away from the combination of geneticism and essentialism that continues to perpetuate the logic of raciology even in the course of its vehement denial. (shrink)

Enormous phylogenetic variation exists in the number and sizes of introns in protein‐coding genes. Although some consideration has been given to the underlying role of the population‐genetic environment in defining such patterns, the influence of the intracellular environment remains virtually unexplored. Drawing from observations on interactions between co‐transcriptional processes involved in splicing and mRNA 3′‐end formation, a mechanistic model is proposed for splice‐site recognition that challenges the commonly accepted intron‐ and exon‐definition models. Under the suggested model, splicing factors (...) that outcompete 3′‐end processing factors for access to intronic binding sites concurrently favor the recruitment of 3′‐end processing factors at the pre‐mRNA tail. This hypothesis sheds new light on observations such as the intron‐mediated enhancement of gene expression and the negative correlation between intron length and levels of gene expression. (shrink)

The serotonin transporter plays an important role in regulating serotonergic transmission via removal of serotonin from synaptic clefts. Alterations in 5-HTT expression and subsequent 5-HT transmission have been found to be associated with changes in behaviour, such as fearfulness or activity, in humans and other vertebrates. In humans, alterations in 5-HTT expression have been suggested to be able to lead to better learning performance, with more fearful persons being better at learning. Similar effects of the variation in the 5-HTT on (...) fearfulness have been found in chickens, and in this study, we investigated effects on learning. Therefore, we tested 52 adult laying hens, differing in their functional 5-HTT genotype in an operant learning paradigm in three different phases and in a tonic immobility test for fearfulness. We found that the 5-HTT polymorphism affects the initial learning performance of laying hens, with homogeneous wild-type hens being the slowest learners, and the most fearful birds. W/W hens, showed significantly more choices to solve the initial learning task and had the highest latencies in a tonic immobility test, indicating the highest fearfulness. Our results provide interesting first insights into the role of 5-HTT in chickens and its sensitive interaction with the environment. We further suggest that the 5-HTT gene can be an interesting target gene for future breeding strategies as well as for further experimental studies. (shrink)

As cells approach S phase, many changes occur to create an environment conducive for DNA synthesis and commitment to cell division. The transcription rate of many genes encoding enzymes involved in DNA synthesis, including the dihydrofolate reductase (dhfr) gene, increases at the G1/S boundary of the cell cycle. Although a number of transcription factors interact to finely tune the levels of dhfr RNA produced, two families of transcription factors, Sp1 and E2F, play central roles in modulating dhfr levels. (...) A region containing several Sp1‐binding sites is required for both regulated and basal transcription levels. In contrast, the E2F‐binding sites near the transcription start site are required only for regulated transcription. A model is presented for the regulation of the dhfr gene which may also pertain to other cell cycle‐associated genes. (shrink)

David Papineau (2003; 2005) has discussed the relationship between social learning and the family of postulated evolutionary processes that includes ‘organic selection’, ‘coincident selection’, ‘autonomisation’, ‘the Baldwin effect’ and ‘genetic assimilation’. In all these processes a trait which initially develops in the members of a population as a result of some interaction with the environment comes to develop without that interaction in their descendants. It is uncontroversial that the development of an identical phenotypic trait might depend on (...) an interaction with the environment in one population and not in another. For example, some species of passerine songbirds require exposure to species-typical songs in order to reproduce those songs whilst others do not. Hence we can envisage a species beginning with one type of developmental pathway and evolving the other type. If, however, the successive evolution of these two developmental pathways were a mere coincidence, selection first favoring the ability to acquire the trait and later, quite independently, favoring the ability to develop it autonomously, then this would not be a distinctive kind of evolutionary process, but merely two standard instances of natural selection. George Gaylord Simpson pointed this out in the paper that gave us the term ‘Baldwin effect’ (Simpson, 1953). The real interest of the Baldwin effect and its relatives lies in the mechanisms which might link the evolution of the two developmental pathways, so that acquiring the trait through interaction with the environment makes it more likely that later generations will evolve the ability to acquire the same trait without that interaction. (shrink)