8.2 Gene expression Flashcards
(117 cards)
1
Q
What are differentiated cells
A
Cells that are specialised for a particular function
2
Q
What is an example of a gene that is permanently switched on
A
Genes for respiratory enzymes
3
Q
What is an example of a gene that can be switched on and off
A
Lac operon, which is a digests lactose in bacteria
4
Q
What are stem cells
A
Undifferentiated cells
5
Q
What can all stem cells do
A
Continually divide
6
Q
What can totipotent stem cells do
A
Divide and produce any type of body cell
7
Q
What can pluripotent stem cells do
A
Divide and differentiate into almost any type of cells
8
Q
What is the only mammalian cell that is totipotent
A
Zygote
9
Q
What plant cells are totipotent
A
All
10
Q
What are multipotent stem cells
A
Divide and differentiate into limited number of cells
11
Q
Where might you find multipotent stem cells in humans
A
Bone marrow
12
Q
What mammalian cells are pluripotent
A
Embryonic
13
Q
What can unipotent stem cells do
A
Divide and differentiate into 1 type of cell
14
Q
What type of mammal would you find multipotent and unipotent stem cells
A
Mature mammals
15
Q
What does iPS cells stand for
A
Induced pluripotent stem cells
16
Q
What type of cell becomes an iPS cell
A
Unipotentn stem cell
17
Q
What happens to the unipotent stem cell to become iPS cells
A
Inducing genes and transciption factors to express themselves
18
Q
Why are iPS cells more valuable than embryonic stem cells
A
iPS cells can limitlessly divide whereas embryonic stem cells can limitly divide
19
Q
What risk arises when using iPS
A
Cancer
20
Q
Why is there a risk of cancer when using iPS cells
A
As the cells can divide limitlessly
21
Q
What type of clone is used to specific produce embryonic stem cells
A
Therapeutic
22
Q
How effective are iPS cells
A
Not that effective and therefore don’t always work
23
Q
What triggers transciption to start
A
The binding of a protein to the DNA
24
Q
What is the name of the site on DNA where the transcription factor binds
A
Promoter region
25
If the transcription factor didn't bind to the DNA at the promoter region, what happens to the gene
The gene is switched off and is not expressed as a protein
26
What does steroid hormone mean in terms of transport across membranes
Lipid soluble so simply diffuse
27
What is the example of the steroid hormone on AQA spec
Oestrogen
28
What is the role of the steroid hormone oestrogen in initiating transcription
- Oestrogen simple diffuse into the cytoplasm of the cell.
- Oestrogen then binds to the transcription factor that is already in the cytoplasm.
- The transcription factor changes shape so is now complementary in shape to the promoter region on DNA
- The binding of the transcription factor stimulates RNA polymerase
29
After oestrogen diffuses into the cell, what happens
Oestrogen binds to the transcription factor
30
What is the effect of oestrogen binding to the transcription factor
The transcription factor changes shape to become complementary to the promoter region
31
What does the shape change in the transcription factor, make the transcription factor complementary to
The promoter region on DNA
32
What does the binding of the transcription factor to the promoter region of DNA stimulate
RNA polymerase
33
Define epigenetics
Ability to control gene expression by factors other than change in DNA base sequence
34
What does epigenetics do the genes
Switches them on and off
35
What are the 2 types of epigenetic modifications
- DNA methylation
- Histone modification
36
What DNA bases usually is methylated
Cytosine
37
What happens to the base when DNA methylation occurs
A methyl group (-CH3) is added to a base
38
What is the effect of DNA methylation
Reduces the ability of the the methylated base to be recognised in transcription so reduces ability of gene to be expressed
39
Why are heavily methylated DNA bases less likely to be transcribed
As transcription factors are less likely to bind
40
What are the 2 types of histone modification
- Histone methylation
- Histone Acetylation
41
With histone methylation, what happens to the affinity between DNA and histones
Increase in affinity
42
What is the effect on the chromatin when the affinity between DNA and histones is high, histone methylation
Chromatin is more condensed
43
When chromatin is more condensed, what does this mean for the genes
The genes are less accessible to transcription factors
44
When genes are less accessible to transcription factors what does this mean
Less likely to be expressed, the gene is essentially switched off
45
What is the name of the marker associated with histone methylation
Silencing
46
What is the affinity like between DNA and histones in histone acetylation
Lower affinity
47
What does low affinity between DNA and histones mean for chromatin
Less condensed
48
When chromatin is less condensed, what does this do to the accessiblity of the gene
More accessible to transcription factors
49
When genes are more accessible to transcription factors, what does this mean in terms of expression
More likely to be expressed, switched on
50
What does amino acids being methylated or acetylated determine
How tightly packed the nucleosome is
51
What does siRNA stand for
Small interfering RNA
52
What is siRNA made from
Formed from dsRNA (double stranded RNA)
53
What does dsRNA stand for
Double stranded RNA
54
What happens to dsRNA to form siRNA
dsRNA is broken into smaller siRNA by an enzyme
55
What bonds does the enzyme the cuts dsRNA, catalyse the hydrolysis of
Phosphodiester bonds
56
Once the siRNA strands are formed, what happens to the strands
The hydrogen bonds between the 2 strands are hydrolysed so a single strand is produced
57
What does the single strand of siRNA do
Combines with an enzyme
58
What is the name of the enzyme the siRNA combines with
RISC
59
What does RISC stand for (not on spec)
RNA induced silencing complex
60
What happens to the siRNA and enzyme
The siRNA guides the enzymes to mRNA where there is complementary base pairs between siRNA and mRNA
61
Once the siRNA and mRNA have formed complementary base pairs, what does the enzyme then do
Enzyme then cuts the mRNA into smaller pieces, hydrolysing the phosphodiester bonds
62
What is the effect of cutting the mRNA into smaller pieces
The mRNA cannot be translated at the ribosome
63
If the mRNA cannot be translated, what is the gene said to be
Silenced as the gene protein is not formed
64
What happens to the smaller pieces of mRNA that cannot be translated
Hydrolysed into individual nucleotides that can be reused
65
What is a tumour
A group of abnormal cells that form a growth
66
What are the 2 types of tumours
- Beign
- Malignant
67
What type of tumours cause harm to the body
All types
68
How may a tumour cause harm
- Blockages, obstructions
- Damage the organs by pressure
69
What is the growth rate of a beign tumour like
Slow
70
What type of molecules do beign tumours make
Adhesion molecules
71
What do the adhesion molecules of a beign tumour result in the formation of
A capsule around the abnormal cells
72
What does the capsule around a beign tumour mean the tumour cannot do
Metastasise, spread out
73
Do the cells or beign tumour tend to be differentiated or undifferentiated
Differentiated
74
Why are beign tumours relatively easy to cut out
Because all the abnormal cells are contained within a capsule
75
Is the impact of a beign tumour localised
Yes
76
What may lead to the formation of a beign tumour
- Inflammation
- Injury
- Diet
- Genetics
- Toxins
- Radiation
77
What is the growth rate of a malignant tumour like
Fast
78
Are tumour cells in a malignant tumour differentiated or undifferentiated
Undifferentiated
79
With the cells being undifferentiated in a malignant tumour, what does this mean they can form
Can generate own blood supply
80
What does the undifferentiated malignant tumour cells secrete
Chemicals which can form the tumours own blood vessels
81
Why does the formation of the tumours own blood vessels mean the malignant tumour cells can metastasise (move)
Can break out from the group of tumour cells and enter the blood supply
82
Why are malignant tumours hard to cut out
As no capsule and the cells can metastasise
83
What might cause a malignant tumour
- UV or x-ray exposure
- Tobacco smoke
- Aspestos
- Processed food
84
In the majority of cases, what is the main reason as to why cancer cells arise
The gene that regulate mitosis mutates
85
What is the name of transcription factors that stimulate gene expression
Activators
86
What is the name of transcription factors that inhibit gene expression
Repressors
87
What is the role of the protoncogenes
Express protein that involves in the initiation of DNA replication and mitosis
88
What are oncogenes
Mutated protoncogenes
89
What do oncogenes cause
Permanent activation of the protein that is involved in the initiation of DNA replication and mitosis
90
What are tumour-suppressors role
Express proteins that slow down cell division and cause apotosis which DNA replication errors are detected
91
What happens when a tumour suppressor gene is mutated
The gene that codes for the protein that slows down cell division is permanently switched off
92
When the protein that slows down cell division is switched off, what is the result
Cell division is uncontrolled
93
When a tumour suppressor gene is mutated apotasis is inhibitied, what is the effect of this
Mutated cells are not identified and therefore programmed cell death does not occur so mutated cells divide and lead to tumour formation
94
Are oncogenes hypomethylated or hypermethylated
Hypomethylated
95
When oncogenes are hypomethylated, what happens to the chromatin
Less condensed chromatin
96
How does hypomethylation of oncogenes lead to permanently switching on the protein that initiates DNA replication and mitosis
- Chromatin is less condensed
- Gene is more accessible to transcription factors
- Increased expression of gene/ the gene is permanently switched on
97
Are tumour suppressor genes hypomethylated or hypermethylated
Hypermethylated
98
How does hypermethylation of a tumour suppressor gene inactivate the gene
- More condensed chromatin
- So gene is less accessible to transcription factors
- Gene is less expressed
- So gene is switched off
99
What do tumour cells in breast tissue do
Produce oestrogen
100
What does the production of oestrogen from the tumour cells in breast tissues do to the size of the tumour, and what is this an example of
- Increase the size of the tumour
- Example of positive feedback
101
How does oestrogen increase the number of tumour cells
- Oestrogen binds to transcription factors
- Transcription factors the bind to the protoncogene
- This then permanently turns on the protonogene
- So DNA replication and mitosis occur uncontrollably
102
What can be used to slow down the tumour growth
Use siRNA which leads to mRNA being cut up so the proteins are no translated
103
BRCA1 and BRCA2 are human genes that code for tumour suppressor proteins.
Mutations in BRCA1 and BRCA2 can cause cancer (lines 1–2). Explain how (3 marks)
1. Change in DNA base sequence/triplet;
2. Change in (sequence of) amino acids
OR
Change in primary/tertiary/3
0 structure;
3. (Results in) rapid/uncontrollable cell division;
104
Effective treatment of ER-positive breast cancers often involves the use of drugs
which have a similar structure to oestrogen (lines 9–10).
Suggest and explain how these drugs are an effective treatment of ER-positive breast
cancers. (3 marks)
1. (Drug) binds to (oestrogen/ER)
receptor;
2. Prevents binding of
oestrogen/hormone;
3. No/fewer transcription factor(s)
bind to promoter
OR
RNA polymerase not
stimulated/activated;
105
Treatment with drugs might be able to reverse the epigenetic changes that cause
cancers (lines 16–17). Suggest and explain how. (3 marks)
1. (Drugs could) increase methylation of
oncogene(s);
2. (Drugs could) decrease methylation of tumour
suppressor gene(s);
3. (Increased) methylation of DNA/gene(s)
inhibits transcription/expression (of genes)
OR
Decreased methylation of DNA/gene(s)
stimulates transcription/expression (of genes);
4. Decreased acetylation of histones inhibits
transcription/expression (of genes)
OR
(Increased) acetylation of histones stimulates
transcription/expression (of genes);
106
Describe how alterations to tumour suppressor genes can lead to the development of tumours (3 marks)
- Increased methylation of tumour suppressor genes
- Mutation in tumour suppressor genes
- Tumour suppressor genes are not transcribed/ expressed
- Results in rapid/ uncontrollable cell division
107
Sometimes, a mutagenic agent causes DNA to break. A different enzyme called ATM binds to the broken DNA. This leads to the activation of a protein coded for by a tumour suppressor gene. The effect of ATM binding is to stop cell division until DNA is repaired. A mutation could result in a person having non-functional forms of the gene that produces ATM. What can you predict about the possible effects of having a non-functional form of ATM (3 marks)
- ATM will not bind to broken DNA
- DNA not repaired/ cell still has broken DNA
- Cell division continues/ tumour forms
- Tumour suppressor gene not effective/ not activated
- May have no effect in diploid/ heterozygous organism
- Which still has a functional ATM/ ATM gene
108
Define what is meant by epigenetics (2 marks)
- Heritable changes in gene function
- Without changes to the base sequence of DNA
109
Explain how increased methylation could lead to a tumour (3 marks)
- Methyl groups could be added to both copies of a tumour suppressor gene
- The transcription of the tumour suppressor gene is inhibited
- Leading to uncontrolled cell division
110
What does oestrogen bind to, DNA or protein
Protein
111
What do methyl groups bind to, DNA or protein
DNA
112
What do acetyl groups bind to, DNA or protein
Protein
113
Give 1 way in which benign tumours differ from malignant tumours (1 marks)
Cells of benign tumours cannot spread to other parts of the body/ metastasise
114
Explain how the methylation of tumour suppressor genes can lead to cancer (3 marks)
- Methylation prevents transcription of gene
- Protein not produced that prevents cell division/ causes cell death/ apoptosis
- No control of mitosis
115
One method of transferring RNAi molecules into cells involves combining these molecules with a lipid. Suggest why this increased uptake of RNAi molecules into cells (1 mark)
- Cell membrane has phospholipid bilayer
- No channel/ carrier proteins for uptake
- No need for channel/ carrier proteins
116
Explain why steroid hormones can rapidly enter a cell by passing through its cell-surface membrane (2 marks)
- Lipid soluble
- Diffuse through phospholipid bilayer
117
Binding of testosterone to an AR changes the shape of AR. This AR molecule now enters the nucleus and stimulates gene expression. Suggest how the AR could stimulate gene expression (2 marks)
- AR is a transcription factor
- Binds to DNA/ promoter
- Stimulates RNA polymerase
