gene-environment interplay Flashcards
what is gene-environment interaction
Individuals genetic predispositions express themselves differently depending on the environment. Also includes epigenetic processes such as methylation.
What is gene-environment correlation
When individuals are in environments compatible with their phenotypes.
What are the three kinds of gene-environment
Passive- when children passively inheret environments from parents and siblings that are compatible with their own genetic predispositions.
evocative- when anyone in the environment reacts to individuals in ways that are compatible with or promote their genetic predispositions.
acitve- when the individual seeks environments that are compatible with their genetic predispoitiond
A study for passive and active rGE
Corrigall et al (2015) provided evidence for passive rGE. This study investigated whether parent’s and children’s personality traits (measured according the Big Five traits) would be related to the duration for which children attended music lessons. Results showed that children’s personality traits predicted the duration of music lessons. Also, it was found that parents ‘openness to experience’ predicted the duration of children’s music lessons, even when the child’s personality was controlled for statistically, suggesting that parents passively expose their children to environments that correspond to their genetic propensity. Researchers point out that the correlation between children’s own personality traits and duration of music lessons demonstrates active gene-environment correlation. This is when individuals actively seek out and create environments correlated with their genetic predisposition. Therefore, a contrast between passive and active correlations is that where passive refers to environments passively provided by parents, active refers to the environment that children seek themselves.
A study for evocative rGE
Burt (2009) noted that previous work had suggested that the serotonergic system plays a key role in “popularity” or likeability. A polymorphism within the 5HT2A serotonin receptor gene (−G1438A) has also been associated with popularity, suggesting that genes may predispose individuals to particular social experiences. Genes do not code for the reactions of others to an individual, rather the genes code for a behaviour that evokes particular responses from people. Burt (2009) conducted a study looking at the trait of ‘rule breaking’ given its prior links to both the serotonergic system and to increased popularity during adolescence. Two samples of previously unacquainted late-adolescent boys completed a peer-based interaction paradigm designed to assess their popularity. Analyses revealed that rule breaking partially mediated the effect of the serotonin receptor gene on popularity, thereby showing that genes predispose individuals not only to particular behaviours but also to the social consequences of those behaviours i.e. there was an evocative gene-environment correlation.
Difference between GE interactions and correlations
Unlike gene-environment correlations which explain how due to three processes, environments are often associated with the individual’s genetic predispositions, gene-environment interaction means that the individual’s genetic predispositions express themselves differently depending on the environment.
Describe epigenetics
Epigenetics is the study of phenotypic trait variations resulting from differences in gene expression which are caused by environmental influences, rather than changes in the genetic code. Epigenetic processes include histone modification and DNA methylation. Two of DNA’s four nucleotides, cytosine and adenine, can be methylated. Methylation is when methyl groups are added to the DNA, which stops transcription of DNA into mRNA. Transcription is the first stage of gene expression, so stopping transcription stops gene expression. Therefore when we talk about a gene being active, we are often referring to whether or not is un-methylated and therefore being transcribed.
Name one animal and two human studies for epigenetics
An example of this is the agouti-protein mice (Cooney et al 2002). Female mice of two strains were fed two levels of dietary methyl supplement or control diet prior to and during pregnancy. As a result of this diet, offspring varied in phenotype, due to the expression of agouti-gene which affects fur colour and weight in mice. Those with the low methyl diet had offspring with unmethylated agouti-genes, who were yellow and obese. Epigenetic processes have also been studied in humans, for example Kaati, Bygren, Pembry & Sjostrom (2007) illustrated that the role of nutrients on epigenetics can be trans-generational in humans. By tracking food availability for paternal grandfathers between the ages of 9 and 13, found that food shortages in the grandfathers’ lives affected the lifespan of their grandchildren. A shortage of food for the grandfather was associated with an extended lifespan in his grandchildren. There are also many studies that look at epigenetic effects on specific genes or loci. For example, investigators have found there to be as many as 100 loci with altered CpG methylation in schizophrenia, indicating epigenetic processes (Connor, 2008).
Study for gene-environment interaction
Some GxE interactions supports a diathesis-stress model, whereby genes may means that genetics risk for developing a particular phenotypic trait is higher when the individual is in a high risk environment. An example of this kind of interaction was found by Caspi et al (2002) who showed that individuals who had the rarer form of the gene which conferred low levels of MAOA were more developed more antisocial behaviour in response to severe maltreatment in childhood compared to those with the same form of the gene who experienced no maltreatment. This shows that individuals with this genetic predisposition (low MAOA levels) are only at increased risk of developing anti-social behaviour when they experienced severe maltreatment as children. Importantly, not all those with the high genetic risk who were exposed to a high risk environment actually exhibited anti-social behaviour, showing that there are many other important non-shared environmental influences involved. Additionally, those with a genotype conferring high levels of MAOA expression who were less likely to develop antisocial problems in response to severe childhood maltreatment. These findings provide evidence that genotypes can moderate children’s sensitivity to environmental insults, thus demonstrating a gene-environment interaction.
