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(8) The control of gene expression > Gene Expression > Flashcards

Gene Expression Flashcards

1
Q

What is a stem cell?

A

A cell that can divide by mitosis an unlimited amount of times so differentiate into new cells

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2
Q

What is a totipotent cell?

A

Totipotent cells can divide and produce any type of body cell. (embryonic stem cells)

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3
Q

What is a pluripotent cell?

A
  • these stem cells can differentiate into a limited number of cells
  • can differentiate into any cell type found in an embryo but are not able to differentiate into extra-embryonic cells.
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4
Q

What is a unipotent cell?

A

These stem cells can only differentiate into the same type of cell
eg. skin cells can only produce skin cells

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5
Q

What is an induced pluripotent stem cell (iPS)?

A
  • iPS cells can be produced from adult body cells using appropriate protein transcription factors
  • These transcription factors cause specific genes to be expressed which dedifferentiate a cell back to its pluripotent state
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6
Q

What are the uses of stem cells?

A
  • Regrow damaged cells in humans
  • Type II Diabetes → stem cells differentiated into insulin producing pancreatic cells
  • Paralysis → stem cells differentiated into nerve cells
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7
Q

Evaluate the use of stem cells in treating human disorders.

A

+ve: great potential to treat a large range of diseases, reduces risk of rejection if developed from individual’s own stem cells, adult stem cells already used successfully
-ve: ethical issues (embryonic), could develop infections when cultured in labs, risk of iPS developing mutations leading to cancer cells, low number of stem cell donors

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8
Q

What is a transcription factor?

A

A protein that controls the transcription of genes by binding to a specific region (promoter region) of DNA.

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9
Q

How do transcription factors work?

A
  1. Enter the nucleus from the cytoplasm through nuclear pores
  2. Bind to the promoter region of a gene
  3. Either allows or prevents transcription taking place
  4. Either allows RNA polymerase to bind to the gene (stimulating transcription/gene expression) or prevents binding (inhibiting transcription/gene expression)
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10
Q

What type of hormone is oestrogen?

A

Steroid hormone

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11
Q

Describe the oestrogen stimulation pathway.

A
  1. Oestrogen (steroid hormone) is lipid soluble therefore can diffuse through cell membrane
  2. Oestrogen binds to the receptor site on the transcriptional factor as its complementary in shape
  3. When bound, oestrogen causes transcriptional factor to change shape, to which TF is now complementary and able to bind to DNA to initiate transcription
  4. Activated transcriptional factor can move through nuclear pores into the nucleus and bind to DNA promotor region
  5. When bound to DNA, RNA polymerase can attach and mRNA is created/ transcription can occur
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12
Q

What is epigenetics?

A

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

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13
Q

What is methylation of DNA?

A

Adding on a methyl group (CH3) to cytosine base in DNA
- increased methylation inhibits transcription

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14
Q

Describe the effect of methylation of DNA.

A
  • Causes nucleosomes to pack tightly together
  • prevents the section of DNA from being transcribed
    GENES ARE NOT EXPRESSED
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15
Q

What is acetylation of histone proteins?

A
  • Acetyl groups (COCH3) can bind to histone proteins on DNA
  • DNA becomes less tightly wound around histone
  • Stimulates transcription
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16
Q

Describe the effect of the acetylation of histones.

A
  • Results in loose packaging of nucleosomes
  • Transcriptional factors can bind to the DNA as the DNA is accessible
    GENES ARE EXPRESSED
17
Q

What is heterochromatin?

A

When DNA is tightly coiled, transcription is inhibited
Can be either:
- Increased methylation of DNA
- Decreased acetylation of histones on DNA

18
Q

What is euchromatin?

A

When DNA is loosely packed & accessible transcription will occur
Can be either:
- Decreased methylation of DNA
- Increased acetylation of histones on DNA

19
Q

What is a tumour suppressor gene?

A
  • Produce proteins which slow down cell division by regulating mitosis and ensures only producing new cells when needed
  • Cause cell death if DNA copying errors are detected
20
Q

What happens if mutation occurs in tumour suppressor gene?

A
  • Tumour suppressor genes becomes non-functioning protein
  • Therefore cell division will continue and mutated cells wouldn’t be identified and destroyed
21
Q

What is an oncogene?

A
  • Mutation of the proto-oncogene
  • Genes that will produce proteins that trigger mitosis to occur
22
Q

How can epigenetics cause cancer?

A
  • Tumour suppressor cells can become hypERmethylated therefore gene is turned off and no longer controlling mitosis
    TUMOURS CAN GROW
  • Oncogenes may be hypOmethylated causing gene to be permanently switched on mitosis is continually occurring even when not needed
23
Q

What is the difference between hypermethylation and hypomethylation?

A

Hypermethylation: increase in methyl groups tightly coiled

Hypomethylation: decrease of methyl groups loose

24
Q

Describe the RNA interference pathway.

A
  1. Double stranded RNA in the cytoplasm is broken up by an enzyme into small interfering RNA and is made single stranded
  2. 1 strand of the siRNA then combines with another enzyme within the cytoplasm, this forms the siRNA-enzyme complex
  3. siRNA- enzyme complex then binds to mRNA that has just been transcribed via complementary base pairing
  4. Once bound, the siRNA cuts up the mRNA
    mRNA sequence cant be translated and polypeptide chain isn’t created
25
Q

What are the two types of tumours?

A
  • Benign
  • Malignant
26
Q

What is meant by metastasise

A

When some of the tumour cells can break off, transport in the bloodstream and spread to other parts of the body (resulting in secondary tumours).

27
Q

What is a benign tumour?

A
  • non cancerous
  • grow slowly
  • doesn’t metastasise
  • surrounded by a capsule, localised
  • don’t usually grow back following removal
28
Q

What is a malignant tumour?

A
  • cancerous
  • rapidly growing
  • metastasise
  • often grow back even after removal
  • not encapsulated
29
Q

Why are malignant tumours so hard to remove?

A
  • Not encapsulated: can grow projections into surrounding tissues and develop a blood supply can now receive O2 & glucose and cells divide rapidly as they’re respiring
30
Q

Factors that affect tumour development:

A
  • oncogenes
  • tumour suppressor genes
  • abnormal methylation:
    (hypermethylation in tumour suppressor gene)
    (hypomethylation in oncogenes)
  • increased oestrogen concentrations
31
Q

What is a proto-oncogene?

A

Normal genes that code for proteins that regulate cell growth & cell differentiation.
- Can mutate to form oncogenes (ability to cause cancer)

32
Q

How does oncogene affect tumour development?

A

Oncogene being permanently activated therefore cells divide continually = excess growth of cells in areas where they aren’t needed

33
Q

How do tumour suppressor genes affect tumour development?

A
  • TSG codes for proteins that regulate cell cycle (DNA repair, slowing mitosis)
  • If a mutation occurs in TSG, produces non-functioning protein, cell division will continue and mutated cells wouldn’t be identified and destroyed
34
Q

How does abnormal methylation affect tumour development?

A

Hypermethylation in TSG:
- increased number of methyl groups
- gene is turned OFF so
- no proteins to regulate cell division and slow down mitosis

Hypomethylation in oncogenes:
- decreased number of methyl groups
- gene is switched ON so lots of proteins being made causing cells to continually divide

35
Q

What are oestrogen dependent breast cancer cells?

A
  • Oestrogen is needed by these tumours to stimulate the expression of cell cycle genes that lead to growth and replication
  • The cancer cells within these tumours have oestrogen receptors that promote cell growth when stimulated by oestrogen
36
Q

How does increased oestrogen concentrations affect tumour development?

A

Oestrogen binds to the transcription factor which activates the genes promoting cell division, leading to tumour formation.

(8) The control of gene expression (4 decks)

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