Topic 8 Exam Questions: The Control Of Gene Expression Flashcards

1
Q

8.1 - Gene Mutations

Explain how a single base substitution causes a change in the structure of this polypeptide (not transcription or translation) (3)

A
  1. Change in (sequence of) amino acids/primary structure
  2. Change in hydrogen/ionic/disulfide bonds
  3. Alters tertiary structure
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2
Q

8.1 - Gene Mutations

What is a substitution mutation? (1)

A

Replacement of a base by a different base (in DNA)

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3
Q

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)

A
  1. (EGCG) bind to active site of DNMT
  2. (DNMT) can’t methylate (promotor region of tumour suppressor gene)
  3. Transcriptional factor can bind (to promotor region)
  4. RNA polymerase (stimulated/activated)
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4
Q

8.2 - Cancer

Describe how alterations to tumour suppressor genes can lead to development of tumours. (3)

A
  1. (Increased) methylation (of tumour suppressor genes)
  2. Mutation (in tumour suppressor genes)
  3. Tumour suppressor genes are not transcribed/expressed OR amino acids sequence/primary structure altered
  4. (Results in) rapid/uncontrolled cell division
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5
Q

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)

A
  1. ATM will not bind to DNA
  2. DNA not repaired
  3. Cell division continues/tumour forms
  4. Tumour suppressor (gene) not effective/activated
  5. May have no effect in diploid/heterozygous (organism)
  6. (Which) still has a functional ATM/ATM gene
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6
Q

8.2 - Cancer

Define what is meant by epigenetics. (2)

A
  1. Heritable changes in gene function
  2. Without changes to the base sequence of DNA
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7
Q

8.2 - Cancer

Explain how increased methylation could lead to cancer. (3)

A
  1. Methyl groups (could be) added to (both copies of) a tumour suppressor gene
  2. The transcription of tumour suppressor genes is inhibited
  3. Leading to uncontrolled cell division
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8
Q

8.2 - Cancer

Give one way in which benign tumour differ from malignant tumours. (1)

A

Cells of benign tumour can’t spread to other parts of the body/metastasise OR
cells of benign tumours can’t invade neighbouring tissues

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9
Q

8.2 - Cancer

Explain how methylation of tumour suppressor genes can lead to cancer. (3)

A
  1. Methylation prevents transcription of gene
  2. Protein not produced that prevents cell division/causes cell death/apoptosis
  3. No control of mitosis
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10
Q

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)

A
  1. Faulty protein recognised as an antigen
  2. T cells will bind to faulty protein/to (this) ‘foreign’ protein
  3. (Sensitised) T cells will stimulate clonal selection of B cells
  4. (Resulting in) release of antibodies against faulty protein.
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11
Q

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)

A

(Cell/memebrane has a) phospholipid bilayer
OR
no channel/carrier protein (for uptake)
OR
No need for channel/carrier protein (for uptake)

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12
Q

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)

A
  1. Lipid soluble
  2. (Diffuse through) phospholipid (bilayer)
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13
Q

8.2 Epigenetics and RNA interference

Suggest and explain why testosterone binds to specific AR (androgen receptor). (2)

A
  1. Has a (specific) tertiary structure/shape
  2. (Structure are) complementary
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14
Q

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)

A
  1. (Receptor is) a transcription factor
  2. Binds to DNA/ promoter
  3. (Stimulates) RNA polymerase
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15
Q

8.2 Epigenetics and RNA interference

Suggest and explain one way epigenetics may affect the age when symptoms of Huntington’s disease start. (2)

A
  1. (Increased) methylation of DNA/gene/allele
  2. Inhibits/prevents transcription
    OR 3. Decreased methylation of DNA/gene/allele
  3. Stimulates/allows transcription
    OR 5. Decreased acetylation of histones
  4. Inhibits transcription
    OR 7. Increased acetylation of histones
  5. Stimulates /allows transcription
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16
Q

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)

A
  1. Cell membranes made from phospholipid
  2. (Detergent) dissolves membranes/phospholipid (bilayer)
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17
Q

8.2 Epigenetics and RNA interference

Explain how ultracentrifugatuon separated protein CENP-W from other molecules. (2)

A
  1. Spin (liquid/supernatant) at (very) high speed
  2. Molecules/ CENP-W separates depending on (molecular) mass/size/density
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18
Q

8.2 Epigenetics and RNA interference

Explain how increased methylation could lead to cancer. (3)

A
  1. Methyl groups (could be) added to (both copies of) a tumour suppressor gene
  2. The transcription of tumour suppressor genes is inhibited
  3. Leading to uncontrolled cell division
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19
Q

8.2 - Stem cells

Suggest how the growth of new blood vessels into damaged heart tissues could increase the rate of repair of tissues. (3)

A
  1. Greater blood supply (to damaged areas)
  2. Bringing more oxygen / glucose for respiration
  3. Brings more amino acids for protein synthesis
  4. For cell repair/mitosis/division
20
Q

8.3 - Genome Projects

Suggest and explain how the viruses became able to infect other species of frog. (2)

A
  1. Mutation in viral DNA/RNA/genome/genetic material
  2. Altered (tertiary structure of the) viral attachment protein
  3. Allows it/attachment protein/virus to bind (to receptors of other species
21
Q

8.3 - Genome Projects

Name two techniques the scientists may have used when analysing viral DNA to determine the viruses were closely related (1)

A
  1. The polymerase chain reaction
    2 . Genetic/DNA fingerprinting
    3 (Gel) electrophoresis
  2. DNA/genome sequencing
22
Q

8.3 - Genome Projects

Determining the genome of a virus could allow scientists to develop a vaccine. Explain how. (2)

A
  1. Scientists could identify proteins (that derive from the genetic code)
    OR could identify the proteome
  2. Could then identify potential antigens (to use in the vaccine)
23
Q

8.3 - Genome Projects

Describe how the B lymphocytes would respond to vaccination against Ranavirus. (3)

A
  1. B cell (antibody) binds to (viral) specific/complementary receptor/antigen
  2. B cell clones OR B cell divides by mitosis
  3. Plasma cells release/produce (monoclonal) antibodies (against the virus)
  4. (B/plasma cells produce/develop) memory cells
24
Q

8.3 - Genome Projects

What is meant by a genome? (1)

A

(All) the DNA in a cell/organism

25
8.3 - Genome Projects Explain why the antibody binds to the transcription factor. (2)
1. (Transcriptional factor/antibody) has a specific tertiary structure/shape 2. Complementary (shape/structure)
26
8.4 - DNA probe and Gel Electrophoresis The scientists used a radioactively labelled DNA probe to show that the cells of tobacco leaves contained the SUT1 (sucrose co-transport protein). Describe how they would do this. (4)
1. Extract DNA and add restriction enzymes 2. Separate fragments using electrophoresis 3. (Treat DNA to) form single strands OR (treat DNA to) expose bases 4. The probe will bind to/hybridise/base pair with the SUT1/ gene 5. Is autoradiography/ X ray film (to show the bound probe)
27
8.4 - DNA probe and Gel Electrophoresis What is a DNA probe? (2)
1. (Short) Single strand of DNA 2. Bases complementary (with DNA/allele/gene)
28
8.4 - DNA probe and Gel Electrophoresis Describe how the DNA is broken down into smaller fragments (2)
1. Restriction enzyme 2. (Cuts DNA at specific) base sequence OR (breaks) phosphodiester bonds OR (cuts DNA) at recognition /restriction site
29
8.4 - DNA probe and Gel Electrophoresis Explain why the DNA is treated to make it single stranded. (1)
(So DNA) probe binds/attaches/anneals
30
8.4 - DNA probe and Gel Electrophoresis What is meant by a non-coding base sequence? (1)
Doesn’t code for amino acid/tRNA/rRNA
31
8.4 - DNA probe and Gel Electrophoresis Name the process by which a base in base sequence is lost (1)
Deletion mutation
32
8.4 - DNA probe and Gel Electrophoresis Give the name of the method they used to clone the DNA in vitro (1)
(The) polymerase chain reaction
33
8.4 - DNA probe and Gel Electrophoresis Explain how DNA probes are used to produce results (3)
1. Probes are single stranded /have a specific base sequence 2. Complementary base sequence on (specific) spacer *spacer is non-coding base sequences OR 3. Complementary/specific to (particular) spacer 4. Binds (to single stranded spacer) and glows /produces light/fluoresce
34
8.4 - DNA probe and Gel Electrophoresis Suggest and explain why it is important to be able to identify the specific strain of M.tuberculosis infect a patient. (2)
1. To see if strain is resistant to any antibiotics 2. Soo can prescribe effective /right antibiotic OR 3. See whether (any) vaccine works against this strain/see which vaccine to use/to produce specific vaccine 4. (So) can vaccinate potential contacts/to stop spread OR 5. Can test other people to see if they have the same strain/trace where people caught TB 6. Allowing control of spread of disease/vaccinate/treat contacts (of people with same strain) before they get TB
35
8.4 - Recombinant DNA describe how enzymes could be used to insert a gene into a plasmid (2)
1. Restriction enzymes cuts plasmid OR restriction enzyme produces ‘sticky ends’ 2. Ligase joins gene/DNA and plasmid OR ligase joins ‘sticky ends’
36
8.4 - Recombinant DNA Suggest and explain how a delayed insertion of a gene could produce offspring of a fish without the desired characteristic(2)
1. Cell division has occurred (before gene added) 2. (Cells producing ) gametes don’t receive the gene
37
8.4 - Recombinant DNA Describe the roles of two named types of enzymes used to insert DNA fragments into plasmids. (2)
1. Restriction (enzyme) to cut plasmid/vector 2. Ligase joins gene/DNA to plasmid/vector
38
8.4 - Recombinant DNA Explain the role of reverse transcriptase (1)
Produces (c)DNA using (m)RNA
39
8.4 - Recombinant DNA Explain the role of DNA polymerase (1)
Joins NUCLEOTIDES to produce (complementary strands/of) DNA
40
8.4 - Recombinant DNA Any DNA in the sample is hydrolysed by enzymes before the sample is added to the reaction mixture. Explain why. (2)
1. To remove any DNA present 2. As this DNA would be amplified/ replicated
41
8.4 - Recombinant DNA Suggest one reason why DNA replication stops in the polymerase chain reaction. (1)
Limited number of primers/nucleotides
42
8.4 - Recombinant DNA The scientists used a variety of primers to detect the presence of different RNA in viruses. Explain why. (2)
1. Base sequences differ 2. (Different) COMPLEMENTARY primers required
43
8.4 - Recombinant DNA Describe how a geneticist would attempt to insert copies of a gene into plasmids (3)
1. Cut plasmid with a restriction endonuclease 2. (So that) both have complementary /sticky ends 3. (Mix together) and add ligase to join the complementary/sticky ends
44
8.4 - Recombinant DNA Suggest why the scientists used a marker gene and why they used the gene. (2)
1. Not all cells would have taken up the plasmid successfully 2. Cells that took up the gene will glow
45
8.4 - Recombinant DNA Describe and explain how the polymerase chain reaction (PCR) is used to amplify a DNA fragment. (4)
1. (Requires DNA fragment) DNA polymerase, (DNA) nucleotides and primers 2. Heat to 95°C to break hydrogen bonds (and separate strands) 3. Reduce temperature soo primers bind to DNA/strands 4. Increase temperature, DNA polymerase joins nucleotides (and repeat method)