Controlling Gene Expression: Gene Expression

Question 1

What is totipotency?

Answer 1

Cells that are undifferentiated, unspecialised so found in an early embryo e.g. fertilised eggs can differentiate into any type of cell

Question 2

What are pluripotent cells?

Answer 2

Embryonic stem cells that can differentiate into almost any type of cell. (These cells are now set on becoming a sing person where as the fertilised egg could still divide to form identical twins)

Question 3

What are multipotent stem cells?

Answer 3

Adult stem cells which can differentiate into a limited number of specialised cell making them tissue specific. These do mitosis to regenerate

Question 4

What are untipotent stem cells?

Answer 4

Cells that can only differentiate into a single type of cell made in adult tissue from multipotent cells

Question 5

How are cells differentiated

Answer 5

By some having genes switched on and others with the same genes switched off. Differentiated cells differ visibly from each other as they produce different proteins. The proteins the cell produces are coded for by the genes that are switched on

Question 6

How can pluripotent cells be used to treat human disorders? Give examples

Answer 6

In therapeutic cloning where the cells can be used to regrow damaged tissue to make single separate organs e.g. cardiac muscle cells could be used to treat damaged cardiac muscle from a heart attack or nerve cells which could be used to treat Parkinson’s or Alzheimer’s disease

Question 7

What does small interfering RNA do and how does it affect gene expression?

Answer 7

Destroys an mRNA molecule that’s has already been transcribed before it’s translated to create a polypeptide chain so by inhibiting mRNA translation, the gene that coded for the mRNA strand is therefor not expressed and switched off as it doesn’t create a polypeptide

Question 8

Give the mechanism of how oestrogen controls gene expression (this is gd for synoptic essay)

Answer 8

1. As oestrogen is a steroid hormone, it’s lipid soluble so diffuses through the cell membrane’s phospholipid bilayer and into the cytoplasm
2. The transcription factors site has a specific base sequence and binds to the oestrogen causing the transcription factor to change shape
3. Oestrogen transcription factor complex binds to a sequence of bases in front of the gene in the promoter site
4. RNA polymerase can now bind to the gene and transcribe mRNA already for translation to synthesise the protein

Question 9

Give the mechanism of small interfering RNA

Answer 9

1. Double stranded RNA
2. This is cut by enzyme into short sections
3. The sing,e stranded pieces of small interfering RNA bind to another enzyme
4. The small interfering enzyme complex CBPs with the target mRNA
5. Target mRNA is cut and destroyed
6. This means the target mRNA’s protein isn’t translated into a polypeptide
   7 . The gene has hence been blocked / not expressed

Question 10

What is epigenetics?

Answer 10

How environmental factors can cause a change in gene expression and cause heritable changes without altering the base sequence of DNA

Question 11

What is the epigenome?

Answer 11

The layer that the chemical tags on DNA histones come from

Question 12

How does acetylation affect gene expression?

Answer 12

Allows the gene to be switched ON (deacetylation opposite process and causes off)

1. Histones are acetyled
2. They spread out
3. Genes/ promoter sites are more accessible
4. Easier for RNA polymerase to bind
5. Allows for transcription / translation

Question 13

How does methylation affect gene expression?

Answer 13

• allows gene to be switched OFF
  1. DNA methyltransferase adds a methyl group to cytosine
  2. DNA histone complex is condensed
  3. This inhibits RNA polymerase so transcription factors can’t bind to the DNA
  4. This causes transcription and so translation to be inhibited

Question 14

What are the key points of benign tumours?

Answer 14

• can grow to a large size
• grow very slowly
• the cell nucleus has a relatively normal appearance
• cells are often specialised
• cells produce adhesion molecules that make them stick together so stay in the tissue they form in
• surrounded by a capsule of dense tissue so remain a compact structure
• much less likely to be life threatening but can still push on vital organs so disrupt their functioning
• localised effects on the body
• usually easily removed by surgery
• rarely reoccur after treatment

Question 15

What’s one similarity between benign and malignant tumours?

Answer 15

They can both grow to a large size

Question 16

What are the key points on malignant tumours?

Answer 16

• can also grow to a large size
• grow rapidly
• cell nucleus is larger and appears darker due to the abundance of DNA
• the cells become unspecialised
• cells don’t produce adhesion molecules so metastasise when they spread to other regions of the body forming secondary tumours
• tumours are not encapsulated so grow projections to surrounding tissue
• more likely to be life threatening as abnormal tumor tissue replaces normal tissue
• effect the whole body e.g. weight loss and fatigue
• removal involves radiotherapy, chemo and surgery
• more frequently reoccur after treatment

Question 17

What’s are the two main types of genes that play a role in cancer

Answer 17

Oncogenes and tumor suppressor genes

Question 18

What are proto oncogenes, how can they cause cancer and how is methylation linked to them?

Answer 18

• genes that promote cell division
• they cause cancer when they go through a mutation which makes them oncogenes which is where they are permanently on and so permanently promote cell division
• cancers that are found to have decreased methylation of DNA show the oncogene

Question 19

What are oncogenes?

Answer 19

Mutated proto oncogenes which permenantly promote cell division and / or tumor suppressor genes which can’t inhibit the cell cycle

Question 20

What do tumour suppressor genes do, when can they cause cancer and how are they affected by methylation?

Answer 20

• stop cell division
• causes cancer when they are switched off in a mutation causing the cells to grow out of control. Some of these cells don’t go through apoptosis and can go on to form tumours
• excessive methylation can lead to the mutation

Question 21

Give an example of tumour suppressor genes

Answer 21

BRACA1 and BRACA2

Question 22

Give the process by which hyper methylation of tumour suppressor genes can lead to cancer

Answer 22

1. Hypermethylation of promoter region of the tumour suppressor gene
2. Tumour suppressor gene switched off
3. Transcription of promoter regions of tumour suppressor gene is inhibited
4. Tumour suppressor gene is switched off / silenced
5. Cell division is increased hence tumour is formed
   This is thought to occur in BRACA1 which can lead to breast cancer

Question 23

Why are older women more likely to get breast cancer

Answer 23

As the production of oestrogen begins to increase in the fat cells of the breasts and white blood cells that are drawn to the tumour that forms increases oestrogen production and so increases cell division more. The tumour forms because oestrogen causes protooncogenes to develop into oncogenes hence breast cancer