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Gene-environment interplay describes how genes and environments work together to produce a phenotype, or observable trait Many human traits are under the influnece of gene-enviorment interplay, and is a key componet in understanding how genes and the enviorment comes togther to impact human devlopment. Examples of gene-environment interplay include gene-environment interaction, gene-environment correlation.[1] Another form of gene-environment interplay is epigenics, which is the study of how the enviorment effects the mechanisms that alter gene expression[2].

In order to study the effect the enviroment has on the expression of the human genome, family-based behavioral genetic research methods such as twin, family and adoption studies. [1] However, the identifcation of genes under environmental influence can be completed through Genome-wide association studies. The study of the gene-environment interplay allows for a deeper understanding of the interactions behind the concepts of nature versus nuture. Enviromental factors are caplable of creating deviations from expected gene expressions, which ultimately impact celluar processes, such as cell signaling, and alter the likelihood of disease.By determining the effects on celluar processes, it will allow for a better understanding the mechanism behind disease and provide insight on how to better treat disease[3].

Types of Gene-Environment Interplay[edit]

Gene-Enviornment Interactions (GxE)[edit]

This type of interplay occurs when genetic factors and environmental factors interact to produce an outcome that cannot be explained by either factor alone.[4] For example, a study found that individuals carrying the genetic variant 5-HTT (the short copy) that encodes the serotonin transporter were at a higher risk of developing depression when exposed to adverse childhood experiences, whereas those with other genotypes (long copy) were less affected by childhood maltreatment.However, there is a caveat as the stressful events may also be caused by predesopition for the individual to put themselves in those situations. [5]

Gene-Environment Correlation (rGE)[edit]

Correlations between an individual's genes and environment can be causal or non-causal.[6] There are three well-documented types of causal gene-environment correlations:[6]

Passive Gene-Environment Correlation[edit]

Certain genes may make a parent more likely to expose their child to a particular environment. Since a child has a decent likelihood of inheriting these genes from their parents, correlations may be found between a child's inherited genes and their childhood environment.[7] These correlations are considered "passive" since the child's environment is being determined by parental decisions rather than by the child's own decisions. For example, parents who have high openness-to-experience, which is a moderately heritable personality trait, are more likely to provide their children with musical training.[8] Consequently, a correlation has been documented between children with more openness-to-experience and their likelihood of receiving musical training as young children.

Active Gene-Environment Correlation[edit]

This occurs when individuals seek out environments that are aligned with their genetic predispositions.[9] For example, one study has found that the tendency of adolescents to select peers that smoke or drink depends on their genetics.[10]

Evocative Gene-Environment Correlation[edit]

This type of gene-environment correlation can emerge when an individual's genetically influenced trait(s) causes others to alter their environment.[9] For instance, one study has shown that children in middle childhood evoke varying degrees of parental control from their mothers depending on their genetically influenced tendency to express autonomy.[11]

Epigenetics[edit]

Epigenetics is one type of gene-environment interplay as it focuses on the changes within a cell as a result of changes within gene expression without altering the genetic code.[12] The source of epigenetic changes can be a result of cellular mechanisms or environmental factors. One instance of an environment impacting gene expression is DNA methylation as a result of smoking during pregnancy. [13] Another environmental exposure that can trigger epigenetic changes is heavy metals like arsenic. This is done through the disturbance of histone acetylation and DNA methylation which is correlated with increased rates of cancer, autoimmune diseases, and neurological disorders. [14]

Pollutants[edit]

Epigenetic modifications can affect gene activity independently of DNA sequence modifications.[15] Air pollution exposure has been associated with decreased DNA methylation levels which is a process crucial for gene regulation. The effects of air polution can be seen in the prenatal enviroment as methylation changed in repsonse to the presense of NO2 and NOx,which are forms of air pollution. When exposed to air pollution, there was a decline in intrauterine growth. While the mechanism is not fully understood, it could involve the formation of reactive oxygen species, leading to oxidative stress and cellular signaling cascade or increased fetal cortisol levels.[16] A consequence of altered DNA methylation is hydroxymethylation, which replaces the methyl group with a hydroxyl group. Hydroxymethylation potentially could disrupt gene expression patterns and contribute to disease development, such as lung cancer.[17] Additionally, exposure to pollutants can exacerbate inflammatory conditions like asthma by inducing inflammation in the airways. This leads to increased cytokine expression and immune cell recruitment.[16] Certain pollutants, such as endocrine-disrupting chemicals (EDC), interfere with hormone signaling pathways and gene expression related to hormone regulation. A certain type of EDC, bisphenol A has been linked to changes in gene expression in reproductive tissues and developmental pathways. [18]

Malnutrition[edit]

Nutrition plays a crucial role in shaping gene expression, which can ultimately impact an individual's phenotype. Fetal malnutrition, for example, has been associated with decreased level DNA methylation, particularly on genes like IGF2, which is involved in insulin metabolism. [19] The alteration in DNA methylation patterns can elevate the risk of developing metabolic disorders and type II diabetes mellitus. [20] Furthermore, prenatal malnutrition can lead to differential DNA methylation of genes related to growth, development, and metabolism. These epigenetic changes increase the likelihood of adverse phenotypes such as obesity and high cholesterol later in life. [21] Malnutrition can also significantly impact gene expression in the small intestine, leading to alterations in nutrient transporters, digestive enzymes, barrier function, immune responses, and metabolic adaptation.[22] Socioeconomic factors such as poverty and minority status may exacerbate the effects of malnutrition. Research indicates that individuals that reside in impoverished communities or those who belong to marginalized racial and ethnic groups may encounter limited access to nutritious food options. [23]

Exercise[edit]

Physical activity induces epigenetic modifications of specific genes, altering their expression profiles. For example, exercise has been linked to increased methylation of the ASC gene, which typically decreases with age. Methylation can compact a gene, decreasing the amount of protein produced from the gene and the ASC gene stimulates cytokine production. Thus, the expression of inflammatory cytokines decreases. This suppression can help prevent the development of chronic inflammation and associated age-related diseases due to excess inflammatory cytokines.[24] However, these epigenetic modifications depend on the intensity and type of exercise and are reversible with the cessation of physical activity.[25]

Early Life Stress

Early life stress encompasses parental absence, abuse, and lack of bonding. These stressors during early childhood have been linked with epigenetic modifications of the Hypothalamic-Pituitary-Adrenal (HPA) axis, which mediates the stress response. Using a rat model of maternal care, research has shown that reduced care between mother and offspring is associated with down regulation of glucocorticoid receptors (GR) in the hypothalamus.[26] GRs play a critical role in the HPA axis by aiding in the restoration of normal physiological state after stress exposure. Down regulation of GRs expression occurs through histone modifications and DNA methylation of the GR gene, resulting in dysregulation of the stress response, including prolonged inflammation and cellular damage. Additionally, numerous studies have linked early life stress with later-life psychiatric disorders, including anxiety and depression, through epigenetic modulation of genes involved in the HPA axis. Socioeconomic disparities, discrimination, and cultural factors prevalent within minority communities can contribute to heightened levels of stress and adversity, impacting gene expression and health outcomes.[27]

Animal Models [edit][edit]

Animal models are a controlled and manipulable environment, in which researchers can investigate the complex interactions between genes and environmental factors, shedding light on various biological and behavioral outcomes.

An orange and black butterfly close up
A butterfly's eyes develop differently in a brighter environment

Research on moths and butterflies has shown that environmental factors like bright sunlight influences their color vision.[28] In environments with more light, they develop more different opsins which allow them to detect light and discern colors. Butterflies depend on color vision to find the correct flowers for their diet and their preferred habitat.

Medical Conditions[edit][edit]

Gene-environment interplay has been found to impact a multiptude of conditions that imact human health. For instance, gene-environment interactions have a prevalent role in mental health disorders; specifically, evidence has found a link to alcohol dependence, schizophrenia, and psychosis. The link to alcohol dependence is potentially influced by a dopamine receptor gene (DRD2) as individuals with TaqI allele may have potentially interactions with this allele and alcohol dependence. This interaction is more prevalent when the indiviual is when under higher stress levels. The impacts on pychosis orginate from a single nucleotide polymorphism (SNP), in the AKT1 gene.This that causes its carriers who regularly use cannabis to be more susceptible to developing psychosis. Additionally, indiviuals that are homozygous for this mutation within AKT1 and use cannabis daily are at an increased susectability of devloping psychotic disorders. For schizophrenia,the Methods of genome wide enviorment studies (GWEIS) and Genome-wide association study (GWAS) are used to determine the loci at enviormental factors used in the determination of GxE . Evidence also supports gene-environment interplay to be connected to cardiovascular and metabolic conditions. These include roles in obesity, pulmonary disease, and diabetes. The rise in the incidence of type II diabetes is suggested to be linked to interactions between diet and the FTO and KCNQ1 genes. Mutations within the KCNQ1 gene effect a pathway that leads a decrease in insulin secretion due to a decline in pancreatic β cells, but within mice fed a high fat diet enhaced the dysfuction within the pancreatic β cells.

References[edit]

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