Topic 8 Exam Questions: The Control Of Gene Expression Flashcards
8.1 - Gene Mutations
Explain how a single base substitution causes a change in the structure of this polypeptide (not transcription or translation) (3)
- Change in (sequence of) amino acids/primary structure
- Change in hydrogen/ionic/disulfide bonds
- Alters tertiary structure
8.1 - Gene Mutations
What is a substitution mutation? (1)
Replacement of a base by a different base (in DNA)
8.2 - Cancer
Throat cancer is caused by increased methylation of promoter region of tumour suppressor gene. Methylation is caused by enzyme DNMT. EGCG is a competitive inhibitor of DNMT and allows daughter cells to produce mRNA from tumour suppressor gene. Suggest how EGCG allows the production of mRNA in daughter cells. (3)
- (EGCG) bind to active site of DNMT
- (DNMT) can’t methylate (promotor region of tumour suppressor gene)
- Transcriptional factor can bind (to promotor region)
- RNA polymerase (stimulated/activated)
8.2 - Cancer
Describe how alterations to tumour suppressor genes can lead to development of tumours. (3)
- (Increased) methylation (of tumour suppressor genes)
- Mutation (in tumour suppressor genes)
- Tumour suppressor genes are not transcribed/expressed OR amino acids sequence/primary structure altered
- (Results in) rapid/uncontrolled cell division
8.2 - Cancer
ATM binds to stop cell division until DNA is repaired. A mutation could result in a person having non-functional forms of gene that produces ATM. What can you predict about the possible effects of having non-functional form if ATM? (3)
- ATM will not bind to DNA
- DNA not repaired
- Cell division continues/tumour forms
- Tumour suppressor (gene) not effective/activated
- May have no effect in diploid/heterozygous (organism)
- (Which) still has a functional ATM/ATM gene
8.2 - Cancer
Define what is meant by epigenetics. (2)
- Heritable changes in gene function
- Without changes to the base sequence of DNA
8.2 - Cancer
Explain how increased methylation could lead to cancer. (3)
- Methyl groups (could be) added to (both copies of) a tumour suppressor gene
- The transcription of tumour suppressor genes is inhibited
- Leading to uncontrolled cell division
8.2 - Cancer
Give one way in which benign tumour differ from malignant tumours. (1)
Cells of benign tumour can’t spread to other parts of the body/metastasise OR
cells of benign tumours can’t invade neighbouring tissues
8.2 - Cancer
Explain how methylation of tumour suppressor genes can lead to cancer. (3)
- Methylation prevents transcription of gene
- Protein not produced that prevents cell division/causes cell death/apoptosis
- No control of mitosis
8.2 - Cancer
MM is caused by a faulty receptor protein in cell-surface membranes. Cells in MM tumours can be destroyed by the immune system. Suggest why they can be destroyed by the immune system. (3)
- Faulty protein recognised as an antigen
- T cells will bind to faulty protein/to (this) ‘foreign’ protein
- (Sensitised) T cells will stimulate clonal selection of B cells
- (Resulting in) release of antibodies against faulty protein.
8.2 Epigenetics and RNA interference
One method of transferring RNAi molecules into cells involves combining these molecules with a lipid. Suggest why this increases uptake of RNAi molecules into cells (1)
(Cell/memebrane has a) phospholipid bilayer
OR
no channel/carrier protein (for uptake)
OR
No need for channel/carrier protein (for uptake)
8.2 Epigenetics and RNA interference
Testosterone is asteroid hormone. Steroid hormones are hydrophobic. Explain why steroid hormones can rapidly enter a cell by passing through its cell-surface membrane. (2)
- Lipid soluble
- (Diffuse through) phospholipid (bilayer)
8.2 Epigenetics and RNA interference
Suggest and explain why testosterone binds to specific AR (androgen receptor). (2)
- Has a (specific) tertiary structure/shape
- (Structure are) complementary
8.2 Epigenetics and RNA interference
The binding of testosterone to a specific receptor changes the shape of the receptor. The receptor now enters the nucleus and stimulates gene expression. Suggest how the receptor stimulates gene expression. (2)
- (Receptor is) a transcription factor
- Binds to DNA/ promoter
- (Stimulates) RNA polymerase
8.2 Epigenetics and RNA interference
Suggest and explain one way epigenetics may affect the age when symptoms of Huntington’s disease start. (2)
- (Increased) methylation of DNA/gene/allele
- Inhibits/prevents transcription
OR 3. Decreased methylation of DNA/gene/allele - Stimulates/allows transcription
OR 5. Decreased acetylation of histones - Inhibits transcription
OR 7. Increased acetylation of histones - Stimulates /allows transcription
8.2 Epigenetics and RNA interference
Scientists began by lysing cells and organelles using detergent that dissolves lipids in water to investigate the role of a protein called CENP-W in mitosis. Suggest how the detergent releases CENP-W from cells. (2)
- Cell membranes made from phospholipid
- (Detergent) dissolves membranes/phospholipid (bilayer)
8.2 Epigenetics and RNA interference
Explain how ultracentrifugatuon separated protein CENP-W from other molecules. (2)
- Spin (liquid/supernatant) at (very) high speed
- Molecules/ CENP-W separates depending on (molecular) mass/size/density
8.2 Epigenetics and RNA interference
Explain how increased methylation could lead to cancer. (3)
- Methyl groups (could be) added to (both copies of) a tumour suppressor gene
- The transcription of tumour suppressor genes is inhibited
- Leading to uncontrolled cell division