Table of ContentsImplications and Models of Genotype x Environment (G x E) InteractionGenotype and Phenotypic VariationG x E ImplicationsEnvironmental StressMolecular EventsExperimental DesignMathematical ModelsBackground GenotypesEnvironmentStudies/ApplicationsGENETIC ENVIRONMENT CORRELATIONEvocative A Gene-Environment Correlation Evocative behavior occurs when an individual's gene-environment interaction (hereditary) behavior evokes an environmental response. For example, the association between marital conflict and depression may reflect the strains that arise when engaging with a depressed spouse rather than a causal effect of marital conflict on depression risk. ActiveActive gene-environment correlation occurs when an individual possesses an inherited inclination to select for environmental exposure. For example, typically extroverted individuals may seek out very different social environments than those who are shy and withdrawn. Quantitative Genetic StudiesTwin and adoption studies have provided much of the evidence for gene-environment correlations by demonstrating that putative environmental measures are heritable. For example, studies of adult twins have shown that desirable and undesirable life events are moderately heritable, as are specific life events and circumstances, including divorce, propensity to marry, marital quality, and social support. Studies in which researchers measured child-specific aspects of the environment have also shown that putative environmental factors, such as parental discipline or warmth, are moderately heritable. Television viewing, peer group orientations, and social attitudes have been shown to be moderately heritable. There is also a growing literature on genetic factors that influence behaviors that pose a health risk, such as alcohol, tobacco, and illegal drug use, as well as risky behaviors. Much like parental discipline, these health behaviors are genetically influenced, but are thought to have environmental effects on disease. To the extent that researchers have attempted to determine why genes and environments are correlated, most of the evidence has pointed to the intervening effects of personality and behavioral characteristics. Environments are heritable because the genotype influences behaviors that evoke, select, and modify environmental characteristics. . Thus, environments less conducive to behavior modification tend to be less heritable. Molecular Genetic Studies Evidence for the existence of gene-environment correlations has recently begun to accumulate through molecular genetic investigations. The Genetics of Alcoholism Collaborative Studies Group reported that a single nucleotide polymorphism in intron 7 of the gamma-aminobutyric acid A2 receptor was associated with alcohol dependence and the condition marital. Individuals with the high-risk GABRA2 variant were less likely to be married, in part because they were at higher risk of antisocial personality disorder and were less likely to be motivated by a desire to please others . There is also molecular evidence for a passive gene-environment correlation. A recent study found that children were nearly 2.5 times more likely to be diagnosed with attention deficit hyperactivity disorder (ADHD) if their mothers were divorced, separated, or never married. InIn this sample, however, mothers with the short allele of the dopamine receptor gene DRD2 were more likely to be divorced, separated, or never marry. Additionally, their children were more likely to have ADHD. Therefore, part of the association between parental marital status and ADHD diagnosis in children in this sample is due to the confounding variable of maternal DRD2 genotype. These two studies also highlighted a gene-environment interaction. MeaningScientists want to know whether exposure to an environmental hazard causes disease. The fact that environmental exposures are heritable means that the relationship between environmental exposure and disease can be confounded by genotype. In other words, the relationship may be spurious, because the same genetic factors could influence both exposure to environmental risks and disease. In such cases, measures to reduce environmental exposure will not reduce the risk of disease. On the other hand, the heritability of exposure to environmental conditions does not in itself mean that environmental factors are not responsible for disease and that a reduction in exposure would therefore benefit individuals with a predisposition. genetics to risky behaviors. the behavior evokes an environmental response. For example, the association between marital conflict and depression may reflect the strains that arise when engaging with a depressed spouse rather than a causal effect of marital conflict on depression risk. ActiveActive gene-environment correlation occurs when an individual possesses an inherited inclination to select for environmental exposure. For example, typically extroverted individuals may seek out very different social environments than those who are shy and withdrawn. Quantitative Genetic StudiesTwin and adoption studies have provided much of the evidence for gene-environment correlations by demonstrating that putative environmental measures are heritable. For example, studies of adult twins have shown that desirable and undesirable life events are moderately heritable, as are specific life events and circumstances, including divorce, propensity to marry, marital quality, and social support. Studies in which researchers measured child-specific aspects of the environment have also shown that putative environmental factors, such as parental discipline or warmth, are moderately heritable. Television viewing, peer group orientations, and social attitudes have been shown to be moderately heritable. There is also a growing literature on genetic factors that influence behaviors that pose a health risk, such as alcohol, tobacco, and illegal drug use, as well as risky behaviors. Much like parental discipline, these health behaviors are genetically influenced, but are thought to have environmental effects on disease. To the extent that researchers have attempted to determine why genes and environments are correlated, most of the evidence has pointed to the intervening effects of personality and behavioral characteristics. Environments are heritable because the genotype influences behaviors that evoke, select, and modify environmental characteristics. . Thus, environments less conducive to behavior modification tend to be less heritable. Molecular genetic studies Evidence for correlationsgenes-environment have recently begun to accumulate through molecular genetic investigations. The Genetics of Alcoholism Collaborative Studies Group reported that a single nucleotide polymorphism in intron 7 of the gamma-aminobutyric acid A2 receptor was associated with alcohol dependence and the condition marital. Individuals with the high-risk GABRA2 variant were less likely to be married, in part because they were at higher risk of antisocial personality disorder and were less likely to be motivated by a desire to please others . There is also molecular evidence for a passive gene-environment correlation. A recent study found that children were nearly 2.5 times more likely to be diagnosed with attention deficit hyperactivity disorder (ADHD) if their mothers were divorced, separated, or never married. In this sample, however, mothers with the short allele of the dopamine receptor gene DRD2 were more likely to be divorced, separated, or never to marry. Additionally, their children were more likely to have ADHD. Therefore, part of the association between parental marital status and ADHD diagnosis in children in this sample is due to the confounding variable of maternal DRD2 genotype. These two studies also highlighted a gene-environment interaction. MeaningScientists want to know whether exposure to an environmental hazard causes disease. The fact that environmental exposures are heritable means that the relationship between environmental exposure and disease may be confounded by genotype. In other words, the relationship may be spurious, because the same genetic factors could influence both exposure to environmental risks and disease. In such cases, measures to reduce environmental exposure will not reduce the risk of disease. On the other hand, the heritability of exposure to environmental conditions does not in itself mean that environmental factors are not responsible for disease and that a reduction in exposure would therefore benefit individuals with a predisposition. genetics to risky behaviors.ActiveQuantitative genetic studiesMolecular genetic studiesImportanceGene-environment interaction occurs when two different genotypes respond in different ways to environmental variations. A reaction standard is a graph that shows the relationship between genes and environmental factors when phenotypic differences are continuous. They can help illustrate GxE interactions. When the reaction norm is not parallel, as shown in the figure below, there is a gene-environment interaction. This indicates that each genotype responds differently to environmental variations. Environmental variations can be physical, chemical, biological, behavioral or life events. Say no to plagiarism. Get Custom Essay on “Why Violent Video Games Should Not Be Banned”?Get Original EssayGenetic Environment Interaction, this graph showing lines that are not parallel, then there is a gene by environment interaction .Implications and Patterns of the Genotype x Environment (G x E) Interaction Although the environment has always been in flux, concerns about the rate of change have become major topics of study for ecologists. The ability, or inability, of organisms to adapt to these changes at the necessary speed determines the continuation, extinction, or evolution of species. The genotype by environment interaction (gxe) can be defined as the differential responseof different genotypes under one or more changes in the environment. When populations are not confined to a single area, individuals must have the genetic makeup necessary to survive in the environment in which they live. This may require a slight difference in insect wing size, or the ability to produce various defense compounds in plants between environments. . Similarly, plant and animal breeders have used the gxe interaction to obtain the highest quality products that will generate the most profit. The purpose of this article is to provide a basic understanding of gxe interactions in terms of potential causes, mathematical models, and practical applications. Genotypic or Phenotypic Variation Variation between species results from either of two phenomena, genotypic or phenotypic variation. Genotypes are hypothesized by observing differential effects on their expression. This implies that the most popular method for determining gxe interaction is to study the resulting phenotypes under the influence of the environment. However, Johannsen suggests that because variation in a trait can result from variation in genotype or environment, variation in both heritable and non-heritable trait cannot be determined by inspecting phenotypes alone. It is important to know an organism's environment and its genetic history. Common environmental factors in gxe studies include temperature, light intensity, and humidity. It is often difficult to distinguish genotypic variations from phenotypic variations. Genotypic variation arises from differences in the genomes of different individuals. Results of directional selection, changing gene frequencies to drive the evolution of a species. The second phenotypic variation occurs when individuals are exposed to different environmental parameters while developing similar genomes. In phenotypic variation, individuals adapt in response to specific environmental changes. Acclimation, for some organisms, can occur multiple times without changing the genetic nature of an individual.G x E Implications The genotype-environment interaction has serious implications for the evolution of species. Lande and Shannon (1996) suggest that in constant or unpredictable environments, genetic variance reduces population average fitness and increases extinction risk. The rate of evolution of the average phenotype in response to selection is proportional to the product of the additive genetic variance of the trait and the intensity of directional selection. In the short term, genetic variability is often less critical than other determinants of a population's persistence. But over time, it can play a decisive role in allowing a population to persist and adapt in a changing environment. Today, conservation efforts have focused on genetic events in small populations. However, long-term preservation of biodiversity requires understanding not only the demographics and genetics of small populations, but also the ecology and evolution of abundant species. Environmental Stress Resistance to stress occurs first at the individual level and involves physiological or behavioral tolerance or adaptability. The subsequent response to increased stress may involve survival of only the best-adapted individuals of the species. Replacements can occur between genera or families after species have experienced and responded to environmental stress (Barrett, 1981). In inconsistent environments,Heterogeneous species belonging to less diverse communities should be more resistant to stress induced by variable environments. Fisher (1977, in Barrett 1981) explains that organisms that have adapted to endure inconsistent environments are more likely to tolerate independent stress than organisms that are only adapted to stable environments. At the population level, resistance to environmental stress is enhanced by polymorphism. Polymorphism increases the likelihood that more tolerant individuals will survive and evolve through combinations of genes present in the population. Population resistance is enhanced by polymorphism because it can result in short-term selection of more tolerant genotypes in stressful environments. Molecular events Haploid species can be highly polymorphic, sexual reproduction and diploidy are not requirements for maintaining genetic variation in natural populations. It is not clear by which, but different selection mechanisms have been questioned regarding their ability to protect alleles at loci. G xe interactions must be extended if selection favors different alleles in varying environments. However, occurrences of gxe do not guarantee changes in fitness rankings that would protect the polymorphisms. Studies of gxe interaction at single loci are rare. However, Dean (1995) attempted to understand how events at the molecular level give rise to gxe interaction in fitness. His study will serve as an illustration of the subject. Using natural and laboratory mutants of the Escherichia coli lactose operon, Dean's experiment targeted the effects of environmental variation on genetic variation. The environmental variation, in this case, was generated by five different galactosides, which are the nutrient that limits growth rates during competition experiments. One-way ANOVA showed a significant difference in fitness between operon strains within each environment. Using a linear additive model, Dean found that fitness changes in environments were due to gxe interactions. With his experimentally verified model for lactose metabolism, a description of fitness in terms of molecular events was possible. For example, strain DD320, which was unable to metabolize any of the galactosides, also had a fitness of 0. This indicates that changes in fitness, which are generated by changes in the distribution of metabolic control, are a potential source of gxe interactions. Experimental Design Studying gxe interactions has proven difficult. Experimental design among researchers has varied due to individual perceptions of how factors should be manipulated. However, continued studies lead to appropriate strategies for carrying out such studies. Phenylketonuria (PKU) is a metabolic disorder in which a rare gene gives rise to mental disability when phenylalanine is present in the diet. The G xe interaction became the mechanism for studying this disease when it was discovered that putting children with the genetic defect on a special diet prevented the effects of the disease. Van den Oord performed PKU gxe studies on individuals using tests with and without parents as controls. This decision was made because a genetic marker is not linked to the PKU gene. Van den Oord pointed out that admixture within parental mating type groups of the population cannot have preferential transmission of one allele ordifferences in means. However, he noted that population mixing between parental mating types may affect differences in allelic frequencies or means.Mathematical ModelsInteractionUsing the simplest model, a 2 x 2 fully factorial design, evaluating the effects of the genotype, the environment and the interaction on the phenotype of the organism are provided (Mather and Jones 1958). When two genotypes appear, there is the possibility of having four phenotypes, P11, P12, P22, P21. -gg = P11 - P12-g = P21 - P22e = P11 - P21-e = P12 - P22ge = P11 - P22-ge = P12 - P21Background genotypes The interaction G xe (g) represents the differential response of genotypes in variable environments; e is the sum or average of g; b represents the regression coefficient (Mather and Caligari 1976). This model focuses on the regression coefficient (b) of the genotype's response to a set of changes (g) and the overall effect of the environment (e) relative to the background genotypes. Mather and Caligari (1976) confirmed that differences in b depend on background genotypes and that heterogeneity is attributable to gene interaction. exw + exs + 2eB)-exw + exs + 2eB) 0Difference2dx - (exw - exs)2dx + (exw - exs) 2dxS.S. Sum (exw + exs + 2eB)2S.S. Diff. (exw - exs)2S.CP (exw - exs)(exw + exs + 2eB) b (exw - exs) / (exw + exs + 2eB)Background -WW -WS -SW -SS eB(e2w + e3w)( e2w + e3s)(e2w + e3w)(e2w + e3s)Studies/Applications Referring to Mather and Caligari (1976), the experimental significance will now be discussed. Mather and Caligari involved eight true breeding lines from Wellington and Samarkland inbred stocks, all under the influence of different temperatures. They were able to confirm their hypothesis that the value of b depends on the background genotype. They also found that when it came to progeny yield, some background genotypes responded to environmental changes in the opposite direction to others. The aim of the study was to produce and confirm the previously stated mathematical model. This study was important not only because of its genetic significance, but also because it used an animal population as well as a model organism. Another animal study focused on commercial production, a major contributor to gxe studies. Here the study of environment and genotype on lean growth, health status and quality of pig took place. This study is important for pork producers so that breeding programs, diets, and management practices can be implemented for optimal pig production. Results include that environment has a significant effect on market weight rate, mortality loss, carcass and pork quality, and pig pH. In plants, gxe studies are also important in natural environments and cultivated populations. Tolerance to ultraviolet B radiation in plants has become a very popular topic among scientists in recent years. Ecotypes of Arabidopsis thaliana were exposed to different levels of UV-B. Ecotypes from high altitudes were found to have a higher tolerance to UV-B than those collected at lower altitudes. Tolerance was measured by observing morphological characters such as plant height, number of shoots, number of branches, rosette diameter, vegetative mass and reproductive mass. With these findings, Arabidopsis thaliana can be used as an indicator species for UV-B radiation levels. If plants at lower elevations begin to die or migrate to even lower elevations, they can serve as a warning of increased UV-B. In.