450+ experts on 30 subjects ready to help you just now
Starting from 3 hours delivery
Gene-environment interaction is when two different genotypes respond to environmental variation in different ways. A norm of reaction 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 norm of reaction is not parallel, as shown in the figure below, there is a gene by environment interaction. This indicates that each genotype responds to environmental variation in a different way. Environmental variation can be physical, chemical, biological, behavior patterns or life events.
Genetic environment interaction, this graph indicating lines that are not parallel, then there is gene by environment interaction.
Although the environment has always been in a state of change, concerns regarding the pace of change have become primary topics of study for ecologists. The ability, or inability, of organisms to adapt to these changes at the speed necessary, determines the continuation, extinction, or evolution of species. Genotype by environment interaction (g x e) can be defined as the differential response of varying genotypes under change(s) in the environment. When populations are not confined to one area, individuals must have the genetic make-up to survive in the environment they live in. This may require a slight difference in wing size of insects, or the ability to produce various defense compounds in plants between environments. Similarly, plant and animal breeders have utilized g x e interaction to yield the highest quality products that will gain the most profit. The purpose of this paper is to provide a basic understanding of g x e interactions in terms of its potential causes, mathematical models, and practical applications.
Variation among species results from either of two phenomena, genotypic or phenotypic variation. Genotypes are assumed by observing differential effects on their expression. This implies that the most popular method of determining g x e interaction is by studying the resulting phenotypes under the influence of the environment. However, Johannsen suggests that because variation in a character may result from variation in either genotype or environment, heritable and non-heritable character variation cannot be determined by only inspecting the phenotypes. It is important to know the environment of an organism and its genetic history. Common environmental factors in g x e studies include temperature, light intensity, and humidity. Distinguishing genotypic and phenotypic variation is often difficult. Genotypic variation originates from differences in the genome of different individuals. Directional selection results, modifying the gene frequencies to lead to the evolution of a species. The second, phenotypic variation occurs when individuals are exposed to different environmental parameters during the development of similar genomes. In a phenotypic variation, individuals adapt in response to specific environmental changes. Acclimation, for some organisms, can occur several times without changing the genetic nature of an individual.
Genotype by environment interaction has heavy implications on the evolution of species. Lande and Shannon (1996) suggest that in constant or unpredictable environments, genetic variance reduces the population mean fitness and increases the risk of extinction. The rate of evolution in the mean phenotype in response to selection is proportional to the product of the additive genetic variance in the character and the intensity of directional selection. In the short-term, genetic variability is often less critical than other determinants of population persistence But over time, it can play the decisive role in allowing a population to persist and adapt in a changing environment. Today, efforts put into conservation have focused on genetic events in small populations. However, long-term preservation of biodiversity requires understanding not only of the demography and genetics of small populations but also the ecology and evolution of abundant species.
Resistance to stress first occurs at the level of the individual and involves physiological or behavioral tolerance or adaptability. Subsequent response to increased stress may involve survival only of the better-adapted individuals of the species. Replacements can occur among genera or families once species have experienced and responded to environmental stress (Barrett 1981). Under inconstant environments, heterogenous species in 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 inconstant environments are more likely to tolerate an independent stress compared to those organisms that are only adapted to stable environments. At the population level, resistance to environmental stress is enhanced by polymorphism. Polymorphism increases the probability that more tolerant individuals will survive and evolve through combinations of genes present in the population. Population resistance is enhanced by polymorphism because it may result in the short-term selection of more tolerant genotypes in stressful environments.
Haploid species can be highly polymorphic, sexual reproduction and diploidy are not requirements for maintaining genetic variation in natural populations. It is unknown by which one, but differing selection mechanisms have been questioned in their capacity to protect alleles at loci. G x e interactions must be extensive if selection favors different alleles in varying environments. However, g x e occurrences do not guarantee changes in fitness rankings that would protect polymorphisms. Studies of g x e interaction at single loci are rare. However, Dean (1995) attempted to provide an understanding of how molecular level events give rise to g x e interaction in fitness. His study will be used as an illustration of the topic. Using natural and laboratory lactose operon mutants of Escherichia coli, Dean’s experiment targeted the effects of environmental variation on a genetic variation. Environmental variation, in this case, was generated by five different galactosides, which is the nutrient that limits growth rates during competition experiments. One-way ANOVA showed a significant difference in fitness among operon strains within each environment. By utilizing a linear additive model, Dean found that changes in fitness across environments were due to g x e interactions. Using 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 g x e interactions.
Studying g x e interactions have proven to be difficult. Experimental design among investigators has varied due to individual perceptions of how factors should be manipulated. However, continuing studies are leading to appropriate strategies for carrying out such studies. Phenylketonuria (PKU) is a metabolic disorder in which a rare gene gives rise to a mental handicap when phenylalanine is present in the diet G x e interaction became the mechanism of study for this disease when it was found that putting children with the genetic defect on a special diet prevented the effects of the disease. Van den Oord produced g x e studies of PKU on individuals using tests with and without parents as controls. This decision was made because a genetic marker is not related to the PKU gene. Van den Oord stressed that mixing within the population’s parental mating type groups, there can be no preferential transmission of an allele or differences in means. However, he noted that population mixing between parental mating types may affect the differences in allele frequencies or means.
Using the simplest model, a 2 x 2 fully factorial design, assessment of the effects of genotype, environment, and the interaction on the phenotype of the organism are provided (Mather and Jones 1958). When two genotypes occur, there is the possibility of four phenotypes, P11, P12, P22, P21.
P11 = g + e + ge
P21 = g = e -ge
P12 = g – e – ge
P22 = g – e + ge -e Mean g -g
g = P11 – P12
-g = P21 – P22
e = P11 – P21
-e = P12 – P22
ge = P11 – P22
-ge = P12 – P21
G x e interaction (g) represents the differential response of genotypes under 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 coefficiency (b) of the genotype’s response to a set of changes (g) and the overall effect of the environment (e) in relation to background genotypes. Mather and Caligari (1976) confirm that differences in b depend on background genotypes and that heterogeneity is attributable to genic interaction.
dx – exw – eB
dx + exw + eB
XsB -dx – exs – eB
-dx + exs + eB -dx
– (exw + exs + 2eB)
-exw + exs + 2eB) 0
2dx – (exw – exs)
2dx + (exw – exs) 2dx
S.S. Sum (exw + exs + 2eB)2
S.S. Diff. (exw – exs)2
S.C.P. (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)
Referring back to Mather and Caligari (1976), the experimental significance will now be discussed. Mather and Caligari involved eight true breeding lines from the Wellington and Samarkland inbred stocks all under the influence of differing temperatures. They were able to confirm their hypothesis that the value of b depends on the background genotype. They also found that in respect to a yield of offspring, some background genotypes were reacting to environmental changes in the opposite direction of others. The intent of the study was to produce and confirm the previously stated mathematical model. This study was not only important for its g x e significance but also because it utilized an animal population as well as a model organism.
Another animal study focused on commercial production, a major contributor to g x e studies. Here, the investigation of environment and genotype on lean growth, health status, and pork quality took place. This study is important to pork producers so that breeding schedules, diets, and management practices can be implemented for optimal pork production. Findings included that the environment has a significant effect on the rate of market weight, death loss, carcass and pork quality, and pork Ph. In plants, g x e studies are also important in natural and cultivated populations. Ultraviolet-B radiation tolerance in plants has become a very popular topic among scientists within recent years. Ecotypes of Arabidopsis thaliana were exposed to varying levels of UV-B. It was found that ecotypes from higher elevations had a higher tolerance for UV-B than those collected from lower elevations. Tolerance was measured by observing morphological characters such as plant height, shoot number, branch number, rosette diameter, vegetative mass, and reproductive mass. Because of these findings, Arabidopsis thaliana can be used as an indicator species for UV-B radiation levels. If plants at lower elevations begin to die off or migrate to even lower elevations, they can serve as warnings of increased UV-B. In a similar study, five semi-arid forage oat varieties were tested under ten environments. Soils remained constant while rainfall varied as the environmental factor. It was found that late varieties had higher dry matter and lower crude protein contents, and forage produced under lower rainfall conditions tended to have more dry matter and crude protein. Studies similar to these can lead to breeding for specific environmental tolerant plants and animals in agriculture and conservation.
Gene-environment correlation (or genotype-environment correlation) is said to occur when exposure to environmental conditions depends on an individual’s genotype.
Gene-environment correlations are a correlation between two traits, e.g. height and weight, which would mean that when one changes, so does the other. Gene-environment correlations can arise from both causal and non-causal mechanisms Genetic variants influence environmental exposure indirectly via behavior. Three causal mechanisms giving rise to gene-environment correlations have been described.
Passive gene-environment correlation refers to the association between the genotype a child inherits from his or her parents and the environment in which the child is raised. Parents create a home environment that is influenced by their own heritable characteristics. Biological parents also pass on genetic material to their children. When the children’s genotype also influences their behavioral or cognitive outcomes, the result can be a spurious relationship between environment and outcome. For example, because parents who have histories of antisocial behavior (which is moderately heritable) are at elevated risk of abusing their children, a case can be made for saying that maltreatment may be a marker for the genetic risk that parents transmit to children rather than a causal risk factor for children’s conduct problems.
Evocative gene-environment correlation happens when an individual’s (heritable) behavior evokes an environmental response. For example, the association between marital conflict and depression may reflect the tensions that arise when engaging with a depressed spouse rather than a causal effect of marital conflict on risk for depression.
Active gene-environment correlation occurs when an individual possesses a heritable inclination to select environmental exposure. For example, individuals who are characteristically extroverted may seek out very different social environments than those who are shy and withdrawn.
Twin 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 life circumstances, including divorce, the propensity to marry, marital quality and social support. Studies in which researchers have 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 all been shown to be moderately heritable. There is also a growing literature on the genetic factors influencing behaviors that constitute a risk to health, such as the consumption of alcohol, tobacco and illegal drugs, and risk-taking behaviors. Like parental discipline, these health-related behaviors are genetically influenced but are thought to have environmentally mediated effects on disease. To the extent that researchers have attempted to determine why genes and environments are correlated, most evidence has pointed to the intervening effects of personality and behavioral characteristics.
Environments are heritable because genotype influences the behaviors that evoke, select, and modify the features of the environment. Thus, environments less amenable to behavioral modification tend to be less heritable.
Evidence for the existence of gene-environment correlations has recently started to accrue from molecular genetic investigations. The Collaborative Studies on Genetics of Alcoholism group has reported that a single-nucleotide polymorphism in intron 7 of the gamma-aminobutyric acid A a2 receptor was associated with alcohol dependence and marital status. Individuals who had the high-risk GABRA2 variant were less likely to be married, in part because they were at higher risk for antisocial personality disorder and were less likely to be motivated by a desire to please others. There is also molecular evidence for passive gene-environment correlation. A recent study found that children were almost 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 possessing the short allele of the dopamine receptor gene DRD2 were more likely to be divorced, separated, or never married. Moreover, their children were more likely to have ADHD. Therefore, part of the association between parental marital status and ADHD diagnosis among children in this sample is due to the confounding variable of maternal DRD2 genotype. Both of these studies also found evidence for gene-environment interaction.
Scientists want to know whether exposure to environmental risk causes disease. The fact that environmental exposures are heritable means that the relationship between environmental exposure and disease may be confounded by genotype. That is, the relationship may be spurious because the same genetic factors might be influencing both exposures to environmental risk and disease. In such cases, measures aimed at reducing environmental exposure will not reduce the risk for the disease. On the other hand, the heritability of exposure to environmental conditions itself does not mean environmental factors are not responsible for disease and so exposure reduction would benefit individuals with a genetic predisposition to risk behavior.
Remember! This is just a sample.
You can get your custom paper by one of our expert writers.Get custom essay
121 writers online
Remember: This is just a sample from a fellow student.
450+ experts on 30 subjects ready to help you just now
Starting from 3 hours delivery
We provide you with original essay samples, perfect formatting and styling
To export a reference to this article please select a referencing style below:
By clicking “Send”, you agree to our Terms of service and Privacy statement. We will occasionally send you account related emails.
Where do you want us to send this sample?
Be careful. This essay is not unique
This essay was donated by a student and is likely to have been used and submitted before
Download this Sample
Free samples may contain mistakes and not unique parts
Sorry, we could not paraphrase this essay. Our professional writers can rewrite it and get you a unique paper.
Please check your inbox.
We can write you a custom essay that will follow your exact instructions and meet the deadlines. Let's fix your grades together!