8 The Control of Gene Expression- Gene Expression Flashcards

1
Q

What are stem cells and what are they capable of?

A

Unspecialised cells; capable of dividing & differentiating into any type of cell

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2
Q

Types of stem cells; what are totipotent cells and their function?

A

-Exist only for a very limited time during embryonic development in mammals (first few cell divisions)
-During development, totipotent cells translate only part of their DNA—> cells remain unspecialised
-Are able to produce any type of body cell, cells of supportive structures like the placenta
-Are the most unspecialised stem cell, specialise into many different cell types

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3
Q

Types of stem cells; what are pluripotent cells and their function?

A

-Totipotent cells develop into pluripotent cells in embryos
-Are able to divide in unlimited numbers & produce any type of cell that makes up body except extra-embryonic cell
-Can be used to treat human disorders

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4
Q

Types of stem cells; what are multipotent cells and their function?

A

-Found in mature mammals
-Can develop into a limited number of cell types

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5
Q

Types of stem cells; what are unipotent cells and their function?

A

-Found in mature mammals
-Can divide to produce new cells but can only produce one type of cell

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6
Q

What is the process of stem cells becoming specialised?

A

-Totipotent cells become specialised in embryonic development
-When become specialised—> only some genes in cell are activated; those are expressed
-If gene is expressed—> transcribed into mRNA & translated into a protein
-Differentiation happens as certain proteins are made
-Presence of certain proteins= cell has become specialised

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7
Q

What are the 3 main sources of stem cells?

A

-Adult stem cells (taken from adult body tissues)
-Embryonic stem cells (taken from embryos)
-Induced pluripotent stem cells (iPS)

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8
Q

What are the benefits of using stem cells in disease?

A

-Can be used to reduce preventable deaths
-Can be used to treat conditions decreasing quality of life

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9
Q

What are the disadvantages of using stem cells?

A

-Obtaining them from embryos is controversial for ethical reasons; some think it is depriving an embryo of life

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10
Q

What are Induced Pluripotent Stem Cells (iPS) produced from?

A

-From a specialised adult somatic (body) cell
-Somatic cells → specialised, can’t be used to treat disease

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11
Q

How are iPS cells produced?

A

-Somatic cells are converted → iPS cells by activating genes using appropriate protein transcription factors
-Makes somatic cells unspecialised, so can treat disease
-Can be made from patient’s own body cells → decreases chance of rejection during transplants

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12
Q

How are stem cells used in bone marrow transplants?

A

-Transplants are used to treat blood & immune disorders
-Bone marrow has multipotent stem cells → can produce all types of blood cell

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13
Q

How are stem cells used in drug research?

A

-Stem cells are used to grow artificial tissues
-Drugs can be tested on the tissues before on humans

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14
Q

How can stem cells be used in developmental biology?

A

-Stem cells used to learn more about how an embryo develops & organs are formed
-Learning about developmental biology can help improve medicine by informing us why organs fail/have abnormalities

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15
Q

How can stem cells be used in potential future research?

A

-Stem cells can be used to make new organs/tissue from transplants
-Can also be used to treat irreversible diseases (eg paralysis)
-Could be injected at site of disorder/ problem & encouraged to differentiate → required specialised cell

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16
Q

What is gene expression controlled by?

A

Transcription factors

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17
Q

What are transcription factors and their function?

A

-Proteins that control gene expression by stimulating/ inhibiting transcription of target genes
-Are made in the cytoplasm & move to nucleus; here, they bind to a specific region of DNA to stimulate/ inhibit gene

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18
Q

What are activators and their function?

A

-Transcription factors that stimulate gene expression
-Promote transcription of genes by interacting w/ enzyme RNA polymerase, allowing it to bind to DNA

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19
Q

What are repressors and their function?

A

-Transcription factors that inhibit gene expression
-Prevent transcription of genes by stopping RNA polymerase from binding to DNA

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20
Q

What are the 2 hormones that can regulate transcription?

A

-Peptide hormones
-Lipid-soluble steroid hormones

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21
Q

How do peptide hormones regulate transcription?

A

-Bind to cell surface membranes, trigger secondary messenger response
-Secondary messenger leads to activation/ inhibitation of transcription of some genes

22
Q

How do lipid-soluble steroid hormones regulate transcription + example of this?

A

-Can pass through phospholipid membrane
-Interact directly w/ DNA to promote/ inhibit gene expression
-Eg; oestrogen

23
Q

What is the process of oestrogen initiating gene transcription?

A

-Oestrogen enters cytoplasm of cell through cell surface membrane; it is lipid-soluble so can pass through phospholipid bilayer
-Binds to receptors on transcription factors in cytoplasm; they change shape
-Transcription factors form receptor-hormone complex, can now enter nucleus
-The complex binds to promoter region of DNA; activates transcription & stimulates protein synthesis

24
Q

What does epigenetic regulation do and what is the impact of this?

A

-Interacts w/ DNA to control access to DNA → alters gene expression w/out actually changing DNA code. Changes can be inherited

25
How is the chromatin formed and what surrounds it?
-DNA in nucleus combines w/ histone proteins → combination = chromatin -Chemical layer surrounds chromatin → epigenome
26
What effect does the Epigenome have on the chromatin?
-Epigenome interacts w/ chromatin, changes its structure -Can cause chromatin to become either: more condensed; prevents transcription factors from binding to DNA so transcription is inhibited or less condensed; allows easier access to transcription factors, promoting transcription
27
What are epigenetic markers and their function?
-Epigenetic markers= groups (e.g. methyl groups) that don’t alter base sequence but influence chromatin structure -Chromatin becomes more/less condensed when epigenetic markers are attached/removed to DNA/histone proteins
28
What happens when there’s increased methylation?
-Methyl groups bind to CpG site (areas in DNA where cytosine & guanine are together in base sequence) on DNA -Methyl groups cause chromatin to be more condensed; transcription factors can’t reach DNA -Methylation inhibits transcription
29
What happens when there’s decreased methylation?
-Acetyl groups (CH3CO) are removed from histone proteins; increases their positive charge & so attraction to phosphate groups on DNA -Decreased acetylation causes chromatin to condense; transcription factors can’t reach DNA
30
How do epigenetic markers influence inheritance?
-Action of epigenetic markers results in changes in chromatin structure -Epigenetic markers can be inherited by offspring -Inheritance of epigenetic control means environmental factors (e.g. methylation) experienced by individual can influence gene expression of offspring
31
When can epigenetics cause disease?
If they aren’t controlled properly
32
Epigenetics; how can abnormal methylation cause disease?
-Epigenetic changes can cause diseases (e.g cancer) -Methyl groups are important in regulating processes like cell division -If methylation isn’t regulated properly, can affect regulation of these important processes
33
Epigenetics; how can increased methylation cause disease?
-Can decrease gene expression of tumour suppressor genes more than normal -Tumour suppressor genes prevent cell division from taking place -If genes are underexpressed, cells divide uncontrollably & tumours are produced
34
Epigenetics; how can decreased methylation cause disease?
-Can increase gene expression of proto-oncogenes (which promote cell division) more than normal -If genes are overexpressed, cells divide uncontrollably & tumours are produced
35
Why can epigenetics treat disease?
Epigenetic markers can be removed easily
36
How can epigenetics change treat disease and how does this impact drugs and therapies?
-Epigenetic changes that cause disease (e.g methylation leading to cancer) = temporary, can be reversed -Ability to reverse epigenetic change= important for designing new drugs + therapies -Researchers are investigating how drugs can reverse silencing/overexpression of genes -Drugs that can reverse epigenetics can help return gene expression to normal level
37
What is translation inhibited by?
RNA interference (RNAi), small molecules of double-stranded RNA
38
How does RNAi influence gene expression?
Interferes w/ mRNA by binding to mRNA molecule, breaking it down; prevents it from being translated into protein
39
What is siRNA and its function?
-Type of RNAi complementary to mRNA sequence it inhibits -Targets specific sequence of mRNA -After siRNA has bound to mRNA, the mRNA is broken down into smaller fragments; which are degraded
40
What is miRNA and its function?
-Not fully complementary to mRNA sequence -Can target multiple sequences of mRNA -After miRNA has bound to mRNA, the mRNA is degraded or stored for future use
41
What do investigations into gene expression provide data on?
Which genes are 'switched on' & which genes are 'switched off'
42
What are DNA microarrays used for?
-Measure gene expression -Used to study extent to which certain genes are expressed in a cell
43
What are tumours and their two types?
-A cluster of cells growing uncontrollably. In some cases, can cause cancer -Benign tumours -Malignant tumours
44
What are the differences between benign and malignant tumours?
-Benign tumours: not cancerous, consist of cells dividing uncontrollably but cannot spread & invade other tissues. Can develop into malignant tumours -Malignant tumours; cancerous, consist of cells dividing uncontrollably & spread into other tissues + around body. Can be life-threatening, grow rapidly
45
When do tumours develop?
When gene expression is not regulated correctly
46
What are tumor suppressor genes and how does their inhibition cause the development of tumours?
-Genes found in all cells; inhibit cell division to regulate rate at which cells divide -Increased methylation of a tumour suppressor gene inhibits this gene; when tumour suppressor genes aren’t expressed, cell division isn’t inhibited: cells divide uncontrollably
47
What are oncogenes and how can they cause development of tumours?
-Mutations in a gene called a proto-oncogene -Are capable of transforming cell into cancerous cell as they cause excessive cell division -Proto-oncogenes normally stimulate cell division; decreased methylation of them causes proto-oncogenes to be over-expressed: stimulates cell division
48
How can oestrogen cause the development of tumours?
-Can increase expression of genes; when they’re over-expressed, a tumour may develop -High levels of oestrogen have been detected in some breast cancers.
49
What are the two factors affecting the development of cancers + examples?
-Environmental factors, including exposure to radiation, smoking, alcohol consumption, eating a diet high in fat -Genetic factors, including having certain alleles
50
What is correlation vs causation in factors affecting the development of cancer?
-Environmental & genetic factors have been found to correlate w/ cancer -Correlations= there’s an association between the two factors -Correlations are different from causes as they don’t always mean a person will develop cancer
51
How can information related to the roles of oncogenes & tumour suppressor genes be used to prevent cancer?
-Understanding what increases chance of creating mutations in oncogenes & tumour suppressor genes (e.g. radiation) can help prevent cancer -Preventative measures can be taken; will reduce the risk of developing cancer -More sensitive tests can be used to diagnose cancers
52
How can information related to the roles of oncogenes & tumour suppressor genes be used to treat cancer?
-If we know what gene mutations cause cancer, drugs can be developed to target these specific mutations -Treatment for cancer can be made more specific by differing drugs according to type of mutation -Intensity of treatment needed can be determined by identifying what mutation= cause -Some mutations are more aggressive, require stronger treatment than others