Gene Expression

Question 1

Mutations and types of mutations?

Answer 1

Mutations are any chance to the base (nucleotide) sequence of DNA.

They can be caused by errors during DNA replication and can be increased by mutagenic agents.

Types:

• Substitution,
• Deletion,
• Addition,
• Duplication,
• Inversion,
• Translocation.

Question 2

Inversion Of Bases?

Answer 2

This mutation occurs on the DNA base sequence but changes the entire chromosome.

What Happens:
- A group of bases become separated from the DNA sequence

Question 3

Substitution?

Answer 3

One or more bases are swapped for another.

ATG > ATC

Question 4

Deletion?

Answer 4

One or more bases are removed.

ATG > AT

This can cause a frame shift.

Question 5

Addition?

Answer 5

One or more bases are added.

ATG > ATGA

Question 6

Duplication?

Answer 6

One or more bases are repeated.

ATG > ATGG

This is different to addition because G is being repeated rather than another random base being added. This is kind of a type of addition though.

Question 7

Inversion?

Answer 7

A sequence of bases is revered.

ATG > GTA

Question 8

Translocation?

Answer 8

A sequence of bases is moved from one location in the genome to another.

This could be a movement within the same chromosome or a movement to a different chromosome.

Question 9

How could a mutation change the amino acid sequence?

Answer 9

The order of DNA Bases codes for the amino acid sequence. So mutations COULD, but not always, change the amino acid sequence.

Polypeptides make up proteins. A change in the sequence for the polypeptides might change the tertiary structure (final 3D shape) of the protein. This could make the protein un-useful.

A mutation in a enzyme may change the shape of the enzymes active site and make it unable to attach to substrates, therefore making it unable to catalyse a reaction.

Question 10

What are genetic disorders and how are they caused?

Answer 10

Some mutations can cause genetic disorders.

Genetic disorders are inherited disorders caused by abnormal genes or chromosomes (e.g. cystic fibrosis).

Some mutations increase the likelihood of developing a certain cancer. E.g. mutation of the gene BRCA1 can increase the chances of developing breast cancer.

Question 11

What are hereditary mutations and how do they occur?

Answer 11

If a gamete (sex cell) containing a mutation for a genetic disorder or a type of cancer is fertilised, the mutation will be present in the new fetus.

This is a hereditary mutation because the mutation has passed onto the offspring.

Sometimes hereditary mutations can be beneficial - they drive evolution.

Question 12

Why do mutations not always effect the order of amino acids?

Answer 12

The degenerate nature of the genetic code means that some amino acids are coded for by more than one DNA triplet.

This means that some mutations will code for the same amino acid and therefore the same polypeptide.

When this happens, it’s called a ‘silent mutation’.

Substitutions do this.
Inversions do this too.

But additions, duplications and deletions will almost always change the amino acid sequence. This is because these mutations change the number of bases in the DNA code which means a frameshift occurs in the bases that follow the mutation.

This means the triplet code is read differently.

Question 13

What are the mutagenic agents and how do they increase mutations?

Answer 13

Mutations occur spontaneously, e.g. when DNA is misread during replication.

Mutagenic agents - anything that increases the rate of mutations.

Examples:

• Ultraviolet light,
• Ionising radiation,
• Some chemicals,
• Some viruses.

They increase rate of mutations by:
- Acting as a base - chemicals called base analogs can substitute for a base during DNA replication. This changes the base sequence in the nee DNA.
E.g. 5-bromouracil is a base analog that substitutes for thymine and but pairs with guanine (instead of adenine) which causes a substitution in the new DNA.

• Altering bases - some chemicals can delete or alter bases. E.g. alkylating agents can add an alkyl group to guanine, which changes the structure so that it pairs with thymine (instead of cytosine).
• Changing the structure of DNA - some types of radiation can change the structure of DNA replication. E.g. UV radiation can cause adjacent (bases next to each-other) thymine bases to pair up together.

Question 14

Mutations in genes?

Answer 14

So we’ve looked at mutations of nucleotide bases and mutations of gametes.
These are mutations of individual cells AFTER fertilisation.

These are called acquired mutations.

Sometimes mutations can occur in genes that control the rate of mitosis which can cause uncontrollable cell division (tumour).

There are two types of gene that control cell division called tumours suppressor genes and proto-onceogenes.

Question 15

What is a tumour?

Answer 15

A mass of abnormal cells.

Tumours that invade and destroy surrounding tissue are cancerous.

Question 16

How can mutations in tumour suppressor genes cause mutations?

Answer 16

Tumour suppressor genes can be inactivated if a mutation occurs in the DNA sequence.

When functioning normally, tumour suppressor genes slow cell division by producing proteins that stop cells dividing or cause them to self-destruct (apoptosis).

If a mutation occurs in a tumour suppressor gene, the protein isn’t produced so the cells divide uncontrollably (the rate of division increases) resulting in a tumour.

Question 17

How can mutations in proto-oncogenes cause mutations?

Answer 17

The effect of proto-oncogene can be increased if a mutation occurs in the DNA sequence.

A mutated proto-oncogene is called an oncogene.

When functioning normally, proto-oncogenes stimulate cell division by producing proteins that make cells divide.

If a mutation occurs in a proto-oncogene, the gene can become overactive. This stimulates the cells to divide uncontrollably (rate of division increases) resulting in a tumour.

Question 18

Two types of tumour?

Answer 18

Malignant tumours - cancerous. They usually grow rapidly and invade and destroy tissues. Cells can break off the tumours and spread to other parts of the body in the blood stream or lymphatic system.

Benign tumours - not cancerous. They usually grow slower than malignant and are often covered in fibrous tissue that stops cells invading other tissues. Benign tumours are often harmless, but they can cause blockages and put pressure on organs. Some of these tumours can become malignant.

Question 19

How do tumour cells differ from normal cells?

Answer 19

Tumour cells have:

1. Irregular shape,
2. The nucleus is larger and darker than normal cells. Sometimes they have more than one nucleus.
3. They don’t produce proteins needed to function correctly.
4. They have different antigens on their surface.
5. They don’t respond to growth regulating processes.
6. They divide by mitosis more frequently than normal cells.

Question 20

What is abnormal methylation?

Answer 20

Methylation means adding methyl (-CH3) group onto something.

Methylation of DNA is an important method for regulating gene expression - it can control whether or not a gene is transcribed (copied into mRNA) and translated (turned into a protein).

When methylation is happening normally, it plays a key role in many processes in the body. However, when it happens too much (hypermethylation) or too little (hypomethylation), it becomes a problem.

The growth of tumours can be caused by abnormal methylation of certain cancer-related genes:
1. When tumour suppressor genes are hypermethylated, the genes are not transcribed. So the proteins they produce to slow cell division aren’t made. This means that cells can divide uncontrollably and tumours can develop.

2. When proto-oncogenes are hypomethylated, they act as oncogenes - increasing the production of proteins that encourage cell division. This stimulates cells to divide uncontrollably which can cause tumours.

Question 21

How can increased oestrogen contribute to breast cancer?

Answer 21

Increased exposure to oestrogen over an extended period of time is thought to increase a woman’s risk of developing cancer.

Increased exposure may be the result of staring mensuration earlier than normal or the menopause later than usual. It could also be the result of taking oestrogen-containing drugs such as HRT.

The reasons behind why this can cause Brest cancer aren’t fully understood but there’s a few theories:
1. Oestrogen can stimulate certain breast cells to divide and replicate. The fact that more cell divisions are taking place naturally increases the chance of a mutation occurring, and so increases the development of cancerous ones.

2. This ability to stimulate division could also mean that if cells do become cancerous, their rapid replication could be further assisted by oestrogen, helping turnouts to form quickly.
3. Other research suggests that oestrogen is actually able to introduce mutations directly into the DNA of certain breast cells, again increasing the chance of these cells becoming cancerous.

Question 22

Risk factors for cancer?

Answer 22

Genetic risk factors - some cancers are linked with specific inherited alleles. If you inherit that allele, your more likely to get that type of cancer (but it doesn’t mean you’ll definitely get it).

Environmental risk factors - exposure to radiation, lifestyle choices like smoking, increased alcohol intake, high-fat diet have all been liked to increased risk of developing cancers.

Question 23

Why is it difficult to draw conclusions on

the causes of cancers?

Answer 23

Data on variation (cancers) can be tricky to interpret because some characteristics can be affected by different genes (they’re polygenic) and many environmental factors.

It’s hard to know what factors are having the greatest effect - or any effect at all.

This makes it hard to drawn conclusions.

E.g. there’s a positive correlation (on graph example in book) between breast cancer in women and number of first-degree relative (mothers, sisters, daughters) who have also had breast cancer. The effect of family history decreases with age, but is still valid. This shows a genetic link.

Another graph shows a positive correlation between both age and breast cancer and another positive correlation between alcohol consumption and breast cancer. Alcohol is a environmental factor.

It’s difficult to tell which factor has the greatest effect (alcohol or genes).

There are other environmental factors (extraneous variables) that are not measured which could have an effect. Like diet and exercise.

Question 24

Why knowing the mutation type is useful for preventing cancer?

Answer 24

Cancer is caused by mutations in proto-oncogenes and tumour suppressor genes.

Understanding the role of these genes in causing cancer and knowing how they work helps us understand ways to prevent it.

1. If a specific cancer causing mutation is known, then it’s possible to screen for the mutation in a persons DNA (e.g. possible to screen for mutated allele for the BRCA1 tumour suppressor gene, which increases woman’s risk of developing breast cancer.
2. Knowing about this increased risk means that prevention steps can be taken. E.g. If we know a woman has the BRCA1 mutation, she can have a mastectomy (removal of one or both breasts) to reduce the risk. Women with this mutation will get regular screening for signs of breast cancer because early diagnosis increases chances of recovery.
3. Knowing about specific mutations also means more sensitive tests can be developed which can lead to earlier diagnosis. E.g. there’s a mutation in the RAS proto-oncogene in around half of all bowel cancers. Bowel cancer can be detected early by looking for the RAS mutations in the DNA of bowel cells.

Question 25

Why knowing the mutation type is useful for treating and curing cancer?

Answer 25

1. The treatment for cancer can be different for different mutations so knowing which one actually caused the cancer can be useful for developing drugs to effectively target them. E.g. breast cancer causes by a mutation of the HER2 proto-oncogene can be treated with a drug called Herceptin. This drug binds specifically to the altered HER2 protein receptor and suppresses cell divisional and tumour growth. Breast cancer caused by other mutations is not treated with this drug cause it doesn’t work.
2. Some cancer-causing mutations require more aggressive treatment than others, so understanding how the mutation that causes them works can help produce the best treatment plan. E.g. if a mutation is known to cause an aggressive (fast growing) cancer, it may be treated with higher doses or radiotherapy or by removing large areas of the tumour and surrounding tissue during surgery.
3. Gene therapy (where faulty genes are replaced by working versions of the alleles) may also be able to treat cancer caused by mutations. E.g. if you know that the cancer is being caused by inactive tumour suppressor genes, it’s hoped that gene therapy could be used.

Question 26

What are stem cells?

Answer 26

Stem cells are unspecialised cells that can develop into any specialised type of cell.

They’re found in the embryo and in some adult tissues.

Stem cells in the intestine cells constantly need replaced epithelial cells.

Question 27

What are totipotent stem cells?

Answer 27

Stem cells that can mature into any type of body cell (including cells that make up the placenta in mammals) are called totipotent stem cells.

They are only present in mammals in the first few cel divisions of the embryo.

After this point, the embryonic (totipotent) stem cells crime pluripotent. They can still develop into any cell in the body but not the placenta.

Question 28

The stem cells present in adult mammals are?

Answer 28

Multipotent stem cells - able to differentiate into a few different types of cell. E.g. both red and white blood cells are formed from multipotent stem cells found in bone marrow.

Unipotent stem cells - can only differentiate into one type of cell. E.g. there’s a type of unipotent stem cell that can only divide to produce epidermal skin cells, which make up the outer layer of your skin.

Question 29

Why do stem cells become specialised?

Answer 29

1. Stem cells all contain the same genes - but during development, not all of them are transcribed and translated.
2. Under the right conditions, some genes are expressed and others are switched off.
3. mRNA is only transcribed from specific genes.
4. The mRNA from these genes is then translated to proteins.
5. These proteins modify the cell - they determine the cell structure and control cell processes (including the expression of more genes, which produce more proteins).
6. Changes to the cell produced by these proteins cause the cell to become specialised. These changes are difficult to reverse. Once specialised, it stays specialised.

Example:
Red blood cells are produced from a type of stem cells in the bone marrow. They contain a lot of haemoglobin and have no nucleus.
The stem cell produces a new cell in which the genes for haemoglobin production are expressed. Other genes such as those involved in removing the nucleus are expressed too. Many other genes not associated with red blood cells are switched off. This makes a red blood cell specialised.

Question 30

What are cardiomyocytes and how are they made?

Answer 30

Heart muscle cells that make up a lot of tissue in heart.

In mature mammals, it’s believed that they cannot divide and replicate.

This meant for ages, we thought that we cannot regenerate new heart tissue if it becomes damaged (heart attack).

But it is now believed that they can regenerate via cardiomyocytes derived from a small supply of unipotent cells in the heart.

Some scientists believe it’s a really slow process and that it’s possible some cardiomyocytes are never replaced. Some believe it’s occurring more quickly so that every cardiomyocyte is replaced several times throughout life.

Question 31

Stem cell therapies that already exist?

Answer 31

Some stem cells therapies already exist for diseases that affect the blood and immune system.

Bone marrow contains stem cells that can become specialised to form any type of blood cell. Bone marrow transplants can be used to record faulty bone marrow in patients that produce abnormal blood cells.

This technique has been used successfully to treat leukaemia (a cancer of blood and bone marrow) and lymphoma (a cancer of lymphatic system). It’s also been used to treat genetic disorders like sickle-cell anaemia and severe combined immunodeficiency (SCID).

Question 32

Example of stem cell therapy?

Answer 32

Severe combined immunodeficiency (SCID) is a genetic disorder that affects the immune system.

People with SCID have poorly functioning immune systems because their white blood cells are defective.

This means they can’t defend the body against infections by identifying and destroying microorganisms.

So SCID suffered are extremely susceptible to infections.

Treatment involved a bone marrow transplant which replaces the faulty stem cells in the bone marrow that is producing the faulty white blood cells. This replaces the genes causing this.

These new stem cells then differentiate to produce functioning white blood cells. These cells can identify and destroy invading pathogens, so the immune system functions properly.

Question 33

How can stem cells be used to treat diseases potentiality in the future?

Answer 33

Spinal cord injuries - stem cells could be used to replace damaged nerve tissue.

Heart disease and damage caused by heart attacks - replace tissue.

Bladder conditions - grow whole bladders, which are then implanted in patients to replace diseased ones.

Respiratory diseases - donated windpipes can be stripped down to their simple collagen structure and then covered with tissue generated by stem cells. This can then be transplanted to patients.

Organ transplants - organs could be grown from stem cells to provide new organs for people on sonar waiting lists.

Question 34

Benefits of using stem cells in medicine?

Answer 34

They could save many lives. People waiting for organ transplants die before the donation becomes available. Stem cells could be used to grow organs for those people awaiting transplants.

They could improve quality of life for many. Stem cells could be used to replace damaged cells in the eyes of people who are blind.

Question 35

Where do we get adult stem cells from?

Answer 35

Adult stem cells are multipotent.

1. Obtained from body tissues of an adult. Stem cells are found in bone marrow.
2. Obtained from simple operation. Little risk is involved but this can be uncomfortable/painful.
3. Adult stem cells aren’t as flexible as embryonic stem cells because they can only specialise into a limited range of cells.

Question 36

Where do we get embryonic stem cells from?

Answer 36

Embryonic stem cells are pluripotent.

1. Obtained from embryos at early stage of development.
2. Embryos are created in a laboratory using Vitro fertilisation (IVF) - egg cells are fertilised by sperm outside the womb.
3. Once the embryos are approximately 4 to 5 days, stem cells are removed from them and the embryo is destroyed.

Question 37

What are induced pluripotent stem cells?

Answer 37

iPS cells are created by scientists in a lab.

This involved reprogramming specialised adult body cells so they become pluripotent.

1. Adult cells are made to express transcription factors (proteins that control whether or not genes are transcribed.
2. The transcription factors cause the adult body cells to express genes that are associated with pluripotency.
3. One of the ways that these transcription factors can be introduced to the adult cells is by infecting them with a specially-modified virus. The virus has the genes coding for the transcription factors within its DNA. When the virus infects the adult cell, these genes are passed into the adult cells DNA and so the cell is able to produce the transcription factors.
4. Induced pluripotent stem cells is so useful but more research needs to be done to properly identify if they are similar enough to true pluripotent embryonic stem cells before they can be used.

(This could cause cancer if the transcriptional factors cause the cells to express oncegenes).

Question 38

Ethical issues surrounding embryonic stem cell use?

Answer 38

1. The use of IVF raises ethical issues because the procedure results in the destruction of an embryo that could become a fetus if placed in womb.
2. Some people believe that the moment of fertilisation means that an individual is formed and has the right to life. They believe it’s wrong to destroy embryos.
3. Some people think that scientists should only use adult stem cells because their production doesn’t destroy embryos. But adult stem cells cannot develop into all types of cell.
4. Less objectivity around stem cells being produced by artificially activating egg cells to divide instead of using sperm.
5. Inducted pluripotent stem cells could be really useful because they have the potential to be as flexible as embryonic stem cells but less ethical issues around this.
6. It is also possible that iPS cells could be made from a patients own cells. These iPS cells will be genetically identical to the patients cells and so they wouldn’t be rejected by immune systems. They wouldn’t be foreign.

Question 39

How do transcription factors control the transcription of target genes?

Answer 39

(Transcription recap - gene is copied from DNA into mRNA. Enzyme responsible is RNA polymerase).

All cells in an organisms carry the same genes but some genes are expressed and some are not.

Transcription of genes is controlled by protein molecules called transcription factors. How?:
1. In eukaryotes, transcription factors move from the cytoplasm to the nucleus.

2. Here, they bind to specific DNA sites near the start of the target genes (genes they control the expression of).
3. They control expression by controlling the rate of transcription.
4. Some transcription factors, called activators, stimulate or increase the rate of transcription. E.g. they help RNA polymerase bond to the start of the target gene and activate transcription.
5. Other transcription factors, called repressors, I hit or decrease the rate of transcription. E.g. they bind to the start of the target gene, preventing RNA polymerase from binding and stopping transcribing.

Question 40

How does oestrogen initiate the transaction of target genes?

Answer 40

1. Oestrogen is a steroid hormone that can effect transcription by binding to a transcription factor called an oestrogen receptor. This form as oestrogen-oestrogen receptor complex.
2. The complex moves from the cytoplasm into the nucleus where it binds to specific DNA sites near the start of the target gene.
3. The complex can act as an activator of transcription, e.g. helping RNA polymerase bind to the start of a target gene.

(In some cells, the oestrogen-oestrogen receptor complex can act as a repressor of transcription instead of an activator. This depends on the type of cell and target gene).

Question 41

RNA interference (RNAi) can inhibit the translation of mRNA?

Answer 41

In eukaryotes, gene expression is also affected by RNAi.

RNAi is where small, double-stranded RNA molecules stop mRNA from target genes being translated into proteins. A similar process to RNAi can also occur in prokaryotes.

The molecules involved in RNAi are called siRNA (small interfering RNA) and miRNA (microRNA).

The process of siRNA in eukaryotes is similar to that of the process of miRNA is in plants.

The process of miRNA in mammals is different.

Question 42

Steps of siRNA (and miRNA

in plants) interfering with mRNA translation?

Answer 42

1. Once mRNA has been transcribed, it leaves the nucleus for the cytoplasm.
2. In the cytoplasm, double-stranded siRNA associates with several proteins and unwinds.
3. A single strand then binds to target mRNA. The base sequence of the siRNA is complementary to the base sequence in sections of the target mRNA.
4. The proteins associated with the siRNA cut the mRNA into fragments - so it can no longer be translated.
5. The fragments then move into a processing body which contains tools to degrade them.
6. A similar process happens with miRNA in plants.

Question 43

Steps of miRNA

in mammals interfering with mRNA translation?

Answer 43

1. In mammals, the miRNA isn’t usually fully complementary to the target mRNA molecule. This makes it less specific than siRNA and so it may target more than one mRNA molecule.
2. Like siRNA, it associates with proteins and binds to target mRNA in the cytoplasm.
3. Instead of the proteins associated with miRNA cutting the mRNA fragments, the miRNA-protein complex physically blocks the translation of the target mRNA.
4. The mRNA is then moved into a processing body, where it can either be stored or degraded. When it’s stored, it can be returned and translated at another time.

Question 44

What is epigenetic control?

Answer 44

In eukaryotes, epigenetic control can determine whether a gene is switched on or off (e.g. ethers the gene is expressed - transcribed and translated - or not).

It works through attachment or removal of chemical groups (called epigenetic marks) to or from DNA or histone proteins.

These epeigentic marks don’t alter the base sequence of DNA.

Instead, they alter how easy it is for the enzymes and other proteins needed for transcription to interact with and transcribe the DNA.

Epigenetic changes to gene expression play a role in lots of normal cellular processes and can also occur in response to changes in the environment - e.g. population and availability of food.

Question 45

How are epigenetic changes inherited?

Answer 45

Organisms inherit their DNA base sequence from their parents.

Most epigenetic marks (tags) on the DNA are removed between generations, but some escape the removal process and are passed on to offspring.

This means that the expression of some genes in the offspring can be affected by environmental changes that affected their parents or grandparents.

For example, epigenetic changes in some plants in response to drought have been shown to be passed on to later generations.

Question 46

How does increasing methylation of DNA switches a gene off?

Answer 46

One method of epigenetic control is methylation of DNA:

1. When a methyl group (an example of an epigenetic mark) is attached to DNA coding for a gene.
2. The group always attaches at a CpG site, which is where a cytosine and guanine base are next to each other in the DNA (linked by a phosphodiester bond).
3. Increased methylation changes the DNA structure so that transcriptional machinery (enzymes, proteins, etc) can’t interact with the gene - so it is not expressed and it’s switched off.

Question 47

How can decreased acetylation of histones also switch genes off?

Answer 47

Histones ate proteins that DNA wraps around to form chromatin, which makes up chromosomes.

Chromatin can be highly condensed or less condensed.

How condensed it is affects the accessibility of the DNA and ethereal or not it can be transcribed.

1. Histones can be epigenetically modified by the addition or removal of acetyl groups (which are another example of an epigenetic mark).
2. When histones are acetylated, the chromatin is less condensed. This means that the transcriptional machinery can access the DNA, allowing genes to be transcribed.
3. When acetyl groups are removed from the histones, the chromatin becomes highly condensed and genes in the DNA can’t be transcribed because the transcriptional machinery can’t physically access them.
4. Histone deacetylase (HDAC) enzymes are responsible for removing the acetyl groups.

Question 48

How can epigenetic lead to the development of diseases?

Answer 48

We’ve already looked at abnormal methylation of tumour suppressor gene and oncogenes and how they can a cause cancer.

Epigenetics can also cause Fragile X syndrome, Angelmans syndrome and Prader-Willi syndrome.

Question 49

How can drugstreat diseases caused by epigenetic changes?

Answer 49

1. Epigenetic changes are revisable, which make them good targets for new drugs to combat diseases they cause.
2. These drugs are designed to counteract the epigenetic changes that cause disease.
3. Increased methylation is an epigenetic change that can lead to a gene being switched off. Drugs that stop DNA methylation can sometimes be used to treat diseases caused by this. E.g. azacitidine is used in chemotherapy for types of cancer that are caused by increased methylation of tumour suppressor genes.
4. Decreased acetylation of histones can also lead to genes being switched off. HDAC inhibitor drugs, e.g. romidepsin, can be used to treat diseases that are caused in this way - including some types of cancer. These drugs work by inhibiting the activity of histone deacetylase (HDAC) enzymes, which are responsible for removing acetyl groups from the histones. Without the activity of the HDAC enzymes, the genes remain acetylated and the proteins they code for can be transcribed.
5. The problem with developing drugs to counteract epigenetic changes is that these changes take place normally in a lot of cells, so it’s important to make sure the drugs are specific. E.g. drugs used in cancer therapies can be designed to only target dividing cells to avoid damaging normal body cells.

5.

Question 50

Influences on phenotypes?

Answer 50

Phenotype of an organism is the result of the interaction of the genotype with the environment.

Overeating - thought to be caused only by environmental factors. It was later discovered that food consumption increases brain dopamine levels in animals. Once enough dopamine was released, people would stop eating. Researchers discovered people with a particular allele had 30% fewer dopamine receptors. They found that people with this particular allele were more likely to overeat - they wouldn’t stop eating when dopamine levels increased. This shows both genetic and environmental causes overeating.

Antioxidants - many foods in our diet contain antioxidants - compounds that play a role in preventing chronic diseases. Science first told us that antioxidant levels in plants differed because of genetic factors. However, we now know that environmental conditions affect the levels of antioxidants. Genetic and environmental factors influence this.

Question 51

Twin studies and how they help determine influences on the phenotype?

Answer 51

Studies of identical twins are extremely useful when trying to determine what’s due to environmental factors and what’s due to genetic factors.

These twins are genetically identical, so any differences in phenotype must be entirely due to environmental factors. If a characteristic is very similar in identical twins, genetics probably plays a more important role.

But if a characteristic is different between the twins, the environment must have a larger influence.

Data coming from twin studies involving a large sample size is better for drawing valid conclusions than data on a small sample size. A large sample size is more representative of the population.