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

Gene Expression Flashcards

(44 cards)

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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

limitation to totipotent cells?

A

-found in early stages of embryo therefore available for a very limited time
- can create tumours in applications (eg testing on a rat) due to nature of stem cells continually dividing

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4
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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5
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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6
Q

What is an induced pluripotent stem cell (iPS)?

A
  • iPS cells can be produced from adult body cells by manipulating the DNA inside the cell by using appropiate transcription factors
  • These transcription factors cause specific genes to be expressed which dedifferentiate a cell back to its pluripotent state
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7
Q

what is meant by the state of pluripotency?

A

when you’ve switched back on all the genes

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8
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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9
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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10
Q

What is a transcription factor?

A

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

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11
Q

what is the structure of a transcriptional factor?

A
  • DNA binding site: will bind to the base sequences on DNA
  • Receptor: Receptor for another molecule to attach to before it can attach to the DNA
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12
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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13
Q

What type of hormone is oestrogen?

A

Steroid hormone

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14
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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15
Q

What is epigenetics?

A

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

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16
Q

what is an epigenome?

A

a single layer of chemical tags on the DNA
- this impacts the shape f the DNA- histone complex and whether the DNA is tightly wound (not expressed) or unwound (expressed)

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17
Q

What is methylation of DNA?

A

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

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18
Q

Describe the effect of methylation of DNA.

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A
  • Causes nucleosomes to pack tightly together
  • prevents the section of DNA from being transcribed
    GENES ARE NOT EXPRESSED
19
Q

What is acetylation of histone proteins?

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A
  • Acetyl groups can bind to histone proteins on DNA
  • DNA becomes less tightly wound around histone
  • Stimulates transcription
20
Q

Describe the effect of the acetylation of histones.

Study These Flashcards
A
  • Results in loose packaging of nucleosomes
  • Transcriptional factors can bind to the DNA as the DNA is accessible
    GENES ARE EXPRESSED
21
Q

What is heterochromatin?

Study These Flashcards
A

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

22
Q

What is euchromatin?

Study These Flashcards
A

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

23
Q

What is a tumour suppressor gene?

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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
24
Q

What happens if mutation occurs in tumour suppressor gene?

Study These Flashcards
A
  • Tumour suppressor genes becomes non-functioning protein
  • Therefore cell division will continue and mutated cells wouldn’t be identified and destroyed
25
what is abnormal methylation?
- methylation can cause gene to turn off/ on - if tumour suppressor gene becomes hypermethylated, causes TSG to tightly coil and gene is turned off - TSG is no longer controlling mitosis/ excess cell growth, so tumours can grow
26
What is an oncogene?
- Genes that will produce proteins that **trigger mitosis** to occur - **Mutation** of the proto-oncogene
27
what happens if oncogene becomes hypomethylated? (decreased methyl groups)
- causes oncogene to be loosely packed SO results in gene being permanently switched on - mitosis is continually occurring even when it isn't needed
28
How can epigenetics cause cancer?
- Tumour suppressor cells can become hyp**ER**methylated therefore gene is turned off and **no longer controlling mitosis** TUMOURS CAN GROW - Oncogenes may be hyp**O**methylated causing gene to be permanently switched on **mitosis is continually occurring even when not needed**
29
What is the difference between hypermethylation and hypomethylation?
Hypermethylation: increase in methyl groups **tightly coiled** Hypomethylation: decrease of methyl groups **loose**
30
what is the point of regulating translation?
when an RNA molecule has already been transcribed, it is destroyed before its translated again, this is done by **siRNA**
31
Describe the RNA interference pathway.
1. Double stranded RNA (dsRNA) in the cytoplasm is cut up into small sections of RNA & is made single stranded by an enzyme and ATP into small interfering RNA (siRNA) 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**
32
how does cancer occur?
result of mutations in genes that regulate mitosis SO uncontrollable cell division and the creation of tumour
33
What are the two types of tumours?
- Benign --> non cancerous - Malignant --> cancerous
34
What is meant by metastasise
When some of the tumour cells can break off, transport in the bloodstream and **spread to other parts of the body** - once tumour has its own blood supply it's getting O2 and glucose SO cells can divide rapidly
35
What is a benign tumour?
- non cancerous - grow slowly - doesn't metastasise - surrounded by a capsule, localised - don't usually grow back following removal
36
What is a malignant tumour?
- cancerous - rapidly growing - metastasise - often grow back even after removal - not encapsulated
37
Why are malignant tumours so hard to remove?
- **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**
38
Factors that affect tumour development:
- **oncogenes** - **tumour suppressor genes** - **abnormal methylation:** (hypermethylation in tumour suppressor gene) (hypomethylation in oncogenes) - **increased oestrogen concentrations**
39
What is a proto-oncogene?
Normal genes that code for proteins that regulate cell growth & cell differentiation. - Can mutate to form oncogenes (ability to cause cancer)
40
How does oncogene affect tumour development?
Oncogene being **permanently activated** therefore **cells divide continually** = **excess growth** of cells in areas where they aren't needed
41
How do tumour suppressor genes affect tumour development?
- 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**
42
How does abnormal methylation affect tumour development?
*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**
43
What are oestrogen dependent breast cancer cells?
- 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
44
How does increased oestrogen concentrations affect tumour development?
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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