Genetics Review & Gene by Environment Interactions

conception/fertilization

ova and sperm unite to form a single cell

what are genes made up of

DNA molecules

what do genes make

proteins

if gene x is turned on, what does it make

protein x

where are pieces of DNA packed into

chromosomes

where are chromosomes packed into

the nucleus of a cell

how many genes do humans have across 46 chromosomes

about 100,000

what chromosomes make someone female

2 x chromosomes

what chromosomes make someone male

1 × 1 y chromosome

what makes everyone different even though everyone has similar genes

inheriting slight differences in sequences of genes

how did mendel discover mendelian genetics

mixing pea plants and even though two traits are present, only one was expressed (if mixing yellow and green peas, you get yellow or green peas, not yellow/green)

what did Mendelian genetics show about seeing traits

some genes allow you to express one, and some don’t allow you to express it

genotype

all traits in a genome

homozygous

similar gene received from each parent

heterozygous

different genes received from each parent

what do many genes have that makes mendelian genetics not as simple

polygenic inheritance, allelic “binding”, random silencing of one allele

behavioral genetics

strategy to understand genetic components to human behavior

how can influence of genetic/environmental factors be distinguished and the influence of each be quantified

using behavioral genetics methods

what do behavioral genetics methods not do

identify specific genes involved

on average, how much DNA do fraternal twins share

50%

what does greater behavioral similarity of identical twins indicate

greater genetic influence on that behavior

what is an advantage of studying twins vs normal siblings

also shows the same environment (uterine, born together, same outside of uterus)

if aggression is highly genetic, how should identical twins be?

equally aggressive

what causes a “unique environment” even for identical twins?

random genetic activity that makes them slightly different

when comparing MZ to DZ twins, what factors are assessed to try and gauge what causes variation?

genetic effects (shared genes), common/shared environment for the twins, unique environment for each twin

What does ACE(R) model stand for

Additive or genetic, Common or shared environment, Environment that is unique, Random error (unexplained factors)

for MZ twins raised in the same family, what are their differences due to?

unique environment

for DZ twins, what would the numerical value be for their genetic correlation

0.5

how much has adding genetic, shared environment, and unique environment been found to contribute to twin correlation?

about 50%

GxE interaction definition

different genotypes respond differently to the same environment, a particular genotype is more sensitive to differences among environments than others

how do we study gene by environment interactions

keep environment of different genotypes constant, keep genotype constant while varying the environment

what accounts for the missing percentage from ACErs being added to 100?

gene by environment interaction

what does gene environment not mean

how much of an impact genes have combined with the environment

even if you are an mz twin and have the same genes for gene x as someone, what happens when you start putting that same genotype in different environments?

it can do better or worse depending on where it is

how do we study GxE interactions?

put all types of the same genome in the same environment and see if some genomes do better, taking identical genomes in different environments and seeing how they react

what did selectively breeding for “bright” and “dull” rats indicate

a genetic basis for individual differences in learning

how did they breed rats into being “bright” and “dull”

bred those with the qualities together until the populations were distinct

how do the bright/dull rats show a strong genetic effect

the offspring were bred to be more like their parents throughout the generations, if the offspring of two bright rats were dull, it would show lack of genetic effect

where do genetically bright rats do better than dull rats

only when raised in the normal/average lab environment

if genetics were the only factor, how would that cause a difference in the bright/dull rats study

in every environment, the bright rats would do better

how did the enriched environment affect the dull rats

they made many fewer errors; intelligence level was super ceded by the environment

what did the bright/dull rats study show

interaction between genome and environment

how did both genotypes react to the environment types

fewer errors in the enriched environment, more errors in the restricted environment

which graph shows no GxE interaction

which graph shows cross-over GxE interaction

which graph shows scalar GxE interaction

what do no interaction graphs mean

doesn’t show that one genotype does better than the other in one environment, regardless of environment, one does better and both genomes equally respond to that environment

what do cross over interaction graphs mean

no main effective genotype, one doesn’t always do better or worse, there is a small environmental effect, there isn’t one gene that is better or worse in all environments, no pure genetic effect that one genome is always better than the other

what is an example of cross over interaction

both genotypes do better in env 2 than 1, small difference because one performed similarly in both environments, orchids and dandelions!

what do scalar interactions graphs show

there is a genetic effect, one genome is always different, and there is an environment effect, one is always different, one genome did better in both environments

what does SNP stand for

single nucleotide polymorphism

SNP

a variation at a single position in a DNA sequence where it differs between alleles in the same location, can happen on almost any gene

Serotonin transporter SNP - how does the presynaptic button allow serotonin to be recycled?

recaptures a lot of released serotonin and puts it in a new vesicle

how much serotonin transporter do short variants make

less of it

how much serotonin transporter do long variants make

more of it

what is the gene/mechanism that recycles the serotonin/repackages the serotonin to be used again

serotonin transporter

what do the variations (S/L) of the serotonin transporter affect

how well reuptake happens

which version of the serotonin transporter allows for more efficient reuptake/recycling of serotonin

long version

which version of the serotonin transporter allows for more efficient reuptake/recycling of serotonin

long version

what happens to serotonin that isn’t recycled

it gets degraded

what does reuptake allow for

serotonin to be captured and used before it degrades, doesn’t need to wait for more to be made

what do SSRIs do

block serotonin reuptake which keeps more serotonin in the synapse, but reduces the pool that can be taken back up

what types of children are more likely to have psychopathology by adolescence and later

maltreated

what is the probability of major depression highly dependent on

genotype of the children

when children experienced no maltreatment, how did genotype affect depressive symptoms

didn’t matter

under maltreatment, what genome (serotonin transporter specifically) was more likely to have depression regardless of probable or severe maltreatment

2 short versions

with no bullying, how much did the genome alone create emotional problems

didn’t create them alone

with occasional bullying, how did bullying affect the likelihood of depression across genomes

increased the likelihood across all genomes

in extreme bullying, how did different genomes react

long version had the lowest likelihood of depression, S/L was medium, S/S had the highest likelihood of depression

how is GxE interaction shown when comparing kids who were bullied vs not

not all three genomes reacted the same or were equally worse off after different severity levels

what type of gene variation has the highest sensitivity to environments

S/S

for kids with at least one S allele for the serotonin transporter gene, what size were their amygdalas

smaller than average

how does amygdala size affect likelihood of depression in children of either early environment with L/L alleles

doesn’t have an impact (dandelion)

for kids with one S allele in high risk environments, what was their amygdala size

smaller than average/shrunk

for children with one s allele in low risk environments, what was their amygdala size

larger than average

regardless of number of stressful life events, how is L/L group in terms of stability and depression

stable, lower level

what happens with S/S serotonin transporter kids as the number of stressful life events increase

worse off, have more proneness to depression

what happens with S/L serotonin transporter kids as the number of stressful life events increase

worse in the worst cases, but the least prone to depressive symptoms if they have fewer stressors (orchid)

how does sensitivity vary in S/L kids depending on environment

sensitivity to the worst in negative ways, sensitivity to the best in positive ways

deletion

we all have the same version of a gene, but some of the building blocks just aren’t there

insertion

somewhere in the gene that matters for the outcome has some extra building blocks, affects how many proteins are made

tandem repeat

we all have the gene for protein x, but for some reason someone has an insertion of random building blocks that are repeated within the genome, can happen a small or large number of times

how does the reading to kids study show the effects of orchid/dandelion relating to the D2 receptor

with the kids with the tandem repeat, have the lowest vocabulary with no reading exposure

when looking for GxE interactions, what is another factor to pay attention to that is often overlooked

age

what happens if you don’t think about genexAge

you don’t know when to look at the environment

what do you need to take into account when looking at GxE at different ages

that at different ages there are different environments (at age 5, genes may play less of a part vs when they’re older)

as adopted children age, who does their IQ more closely resemble

biological parents

what does IQ correlating more with biological parents as children age show about GxE interaction

genes are very prevalent

GE Correlation

in some environments, genes are more likely to be there rather than genes being randomly found in a particular gene; genetic tendencies influence the likelihood of encountering or creating certain environmental conditions

passive GE correlation

parents transmit genes and environment to their children; because environments provided/created by parents depend on those parents’ genotypes, environments will be matched to the child’s genotype

evocative GE correlation

people (parents and others) provide an environment for the child that is based on the child’s genotype; the child’s genetic characteristics affect the behavior of others toward the child

what is an example of an evocative GE correlation

if a child has a crabby gene and frowns more, possibly less likely to be picked up and laughed with, feeds into itself; gene is controlling what the child gets

active GE correlation

children select or create their own environments based on their genotype; environments that children prefer and seek out are those most compatible with their genetic predispositions