8 - Control Of Gene Expression Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What are mutagenic agents

A

Increase the rate of gene mutation
Eg: ionising radiation & carcinogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Explain how a single base substitution causes a change in polypeptide structure

A
  • change in sequence of amino acids/primary structure
  • change in hydrogen bonds
  • alters tertiary structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a substitution mutation

A

1 base replaced with another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can mutations lead to the production of a non-functional protein/enzyme

A
  • change in base sequence of DNA
  • changes sequence of codons on mRNA
  • changes sequence of amino acids in primary structure
  • changes position of hydrogen bonds
  • changes tertiary structure so active site changes shape
  • no ESC’s can form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can a chemical stop the enzyme that causes methylation

A
  • it can bind to the active site of the enzyme
  • so that the enzyme cannot methylate
  • transcription factors can bind to the promoter region
  • so less methylation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the definition of epigenetics

A

Heritable changes in gene function without changes to the base sequence of DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can increased methylation cause cancer

A
  • methyl groups added to both copies of a tumour suppressor gene
  • the transcription of tumour suppressor genes is inhibited
  • leading to uncontrollable cell division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does oestrogen bind with

A

Protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do methyl groups bind with

A

DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do Acetyl groups bind with

A

Protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give one way benign tumours differ from malignant tumours

A

Cells of benign tumours cannot spread to other parts of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain how the methylation of tumour suppressor genes can lead to cancer

A
  • methylation prevents transcription of genes
  • protein is not produced that prevents cell division
  • no control of mitosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why can cells in tumours be destroyed by the immune system 4m

A
  • the faulty protein recognised as an antigen
  • T cells will bind to the faulty protein
  • T cells stimulate clonal selection of B cells
  • so antibodies are released against the faulty protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can a molecule stimulate gene expression

A
  • it can be a transcription factor
  • which will bind to the promoter
  • stimulates RNA polymerase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are unspecialised stem cells capable of

A
  • self renewal
  • can develop into other cells (specialisation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 4 types of stem cells

A
  • totipotent
  • pluripotent
  • multipotent
  • unipotent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe stem cells specialisation

A
  • there is a stimulus
  • causes selective activation of genes
  • mRNA only transcribed from active genes
  • proteins that are translated modify the cell permanently and determine it s function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe totipotent stem cells

A
  • occur for a limited time in early mammalian embryos
  • can differentiate into every cell type in the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe Pluripotent stem cells

A
  • found in embryos
  • can differentiate into most cell types (not cells of the placenta)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe multiplotent stem cells

A
  • found in mature mammals
  • can differentiate into a limited number of cell types
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe Unipotent stem cells

A
  • found in mature mammals
  • can differentiate into only one cell type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are induced pluripotent stem cells produced

A
  • produced from adult somatic cells
  • specific protein transcription factors associated with pluripotency put into cells causing the cell to express genes associated with pluripotency
  • cells are cultured
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why are induced pluripotent stem cells used instead of embryonic cells

A
  • no immune rejection as can be made using patients own cells
  • more ethical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are arguments for the use of embryonic stem cells in treating humans

A
  • Tiny ball of cells, incapable of feeling pain, not equivalent to a human
  • Would otherwise be destroyed (if from infertility treatment which creates more
    than needed)
  • Duty to apply knowledge to relieve human suffering
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are arguments against the use of embryonic stem cells in treating humans

A
  • Embryo is a potential human; should be given rights
  • Induced pluripotent stem cells – cannot yet reliably reprogramme stem cells
  • Could begin to multiply out of control, and cause tumours
26
Q

What are transcription factors

A
  • proteins that move from cytoplasm → nucleus
  • Bind to DNA at a specific DNA base
    sequence on a promotor region
  • they either Stimulate or inhibit transcription of target gene(s) by helping or preventing RNA polymerase binding
27
Q

Why can oestrogen diffuse across the phospholipid bilayer

A

It’s lipid soluble

28
Q

How does oestrogen initiate transcription

A
  • In cytoplasm, oestrogen binds to a
    receptor of an inactive transcription factor, (ITF) forming a hormone-receptor complex
  • the ITF changes shape causing it to become an ACTIVE transcription factor
  • it then diffuses into nucleus and binds to a specific DNA base sequence on a promotor region
  • stimulates transcription of genes by helping RNA polymerase to bind
29
Q

What is the nucleosome ?

A

DNA wrapped around histone proteins
- how closely the DNA and histone are packed together affects transcriptor

30
Q

What are the two types of epigenetic change

A
  • methylation of DNA
  • decreased acetylation of associated histones
31
Q

Describe methylation of DNA

A
  • methyl groups added to cytosine bases in DNA
  • Nucleosomes pack more tightly together → prevents transcription
    factors binding; genes not transcribed (RNA polymerase can’t bind)
  • methylation is Irreversible
32
Q

Describe decreased acetylation of associated histones

A
  • Decreased acetylation of increases positive charge of histones
  • Histones bind DNA (which is negatively charged) more tightly→
    preventing transcription factors binding; genes not transcribed
  • is Reversible
33
Q

How can cancer be detected early from epigenetic change

A

Abnormal levels of methyl and acetyl

34
Q

What is RNA interference (RNAi)

A

RNA molecules inhibit translation of mRNA produced by transcription

35
Q

What are the two genes that can cause development of tumours?

A

Tumour suppressor genes and proto-oncogenes

36
Q

Describe how tumours suppressor (TS) genes could be part of tumours developing

A

1 - Mutation alters primary and tertiary structure of protein - non functional protein
2 - increased methylation prevents transcription of TS genes so uncontrolled cell division

37
Q

Describe how Proto-oncogenes could be part of tumours developing

A

1- Mutation could turn it into permanently activated oncogene
2- decreased methylation or increased acetylation causes excess transcription so uncontrolled cell division

38
Q

What is the normal function of proto-oncogenes?

A

Stimulating cell division

39
Q

What is the normal function of tumour suppressor genes?

A

Decrease cell division
- Causing self destruction of cells, (apoptosis)

40
Q

Describe the role of increased oestrogen concentrations in development of breast cancer

A

At areas of high oestrogen conc - cell division is uncontrolled

41
Q

What is the definition of a genome?

A

The complete set of genes in a cell

42
Q

How can sequencing projects be used on simple organisms?

A
  • Easy because less non-coding DNA
  • identify the antigens on the surface of viruses, which can help develop vaccines
43
Q

Why are sequencing projects on complex organisms harder to use

A
  • Non-coding DNA
  • Regulatory genes
44
Q

What are DNA probes

A
  • short single stranded pieces of DNA
  • bases complementary with DNA
45
Q

Why are probes longer than just a few bases

A
  • a sequence of a few bases would occur at many places throughout the genome
  • longer sequences only likely to occur in target allele
46
Q

Describe DNA hybridisation

A
  • binding of a single stranded DNA probe to complementary single strand of DNA
  • forming hydrogen bonds
47
Q

What are benefits of screening people for genetic conditions and drug responses

A
  • can allow people to make better lifestyle choices
  • people can decide whether to have their own biological children
48
Q

What are drawbacks of screening people for genetic conditions and drug responses

A
  • screening for an incurable disease may be pointless and cause unnecessary stress for someone
49
Q

What are 3 features of proteins that allow them to be separated by gel electrophoresis

A
  • by mass of amino acids
  • charge
  • R groups differ
50
Q

Describe and explain how the polymerase chain reaction (PCR) is used to amplify a DNA fragment 4m

A
  • it requires DNA fragment, DNA polymerase, nucleotides and primers
  • heat to 95C° to break hydrogen bonds and separate strands
  • reduce temperature so primers bind to DNA
  • increase temperature, DNA polymerase joined nucleotides
51
Q

Describe how enzymes could be used to insert a gene into a plasmid

A
  • restriction endonucleases cuts plasmid
  • ligase joins gene to plasmid
52
Q

What’s the role of reverse transcriptase and DNA polymerase in PCR

A

reverse transcriptase produces DNA using mRNA
DNA polymerase joins nucleotides to produce DNA

53
Q

Why is DNA hydrolysed before the sample is added to the reaction mixture in PCR

A
  • to remove any DNA present
  • as this DNA would be amplified
54
Q

Describe the process of inserting genes into plasmids 3m

A
  • cut the plasmid with restriction endonuclease
  • so both have sticky ends
  • mix and add ligase to join the sticky ends
55
Q

What’s the role of siRNA

A
  • destroys mRNA for gene
  • prevents translation of gene
56
Q

What is the name of the method used to clone DNA in vitro

A

Polymerase chain reaction (PCR)

57
Q

Why are a variety of primers used in PCR

A
  • base sequences differ
  • so different complementary primers needed
58
Q

What is the gene machine method of producing DNA fragments

A
  • synthesises fragments of DNA from scratch without the need for a pre existing DNA template
  • DNA fragments produced quickly/accurately
  • free of introns
59
Q

What are the advantages of using mRNA to make DNA fragments rather than restriction enzymes to cut the gene

A
  • more mRNA in the cell than DNA so easily extracted
  • introns removed by splicing whereas DNA contains introns
  • bacteria cannot remove introns
60
Q

How can DNA fragments be produced using mRNA

A
  • isolate mRNA from the cell
  • mix mRNA with DNA nucleotides and reverse transcriptase
  • reverse transcriptase uses mRNA as a template to synthesise a single strand of cDNA
  • DNA polymerase forms second strand of DNA using cDNA as a template
61
Q

What is the role of promoter and terminator regions in vivo

A

Promoter - DNA sequences that tell RNA polymerase when to start producing mRNA

Terminator - tell RNA polymerase when to stop