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Biology A2 > Control of Gene Expression - Transcription and Cancer > Flashcards

Control of Gene Expression - Transcription and Cancer Flashcards

1
Q

what stimulates DNA to start transcription?

A

transcription factors

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2
Q

which genes will transcriptional factors stimulate transcription for?

A

genes switched on only

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3
Q

what can activate transcription factors?

A

oestrogen

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4
Q

how does oestrogen activate transcriptional factors?

A

diffuses through cell membrane and binds with complementary transcriptional factor in cytoplasm

transcriptional factor changes shape

enters nucleus through a pore

binds with DNA at specific base sequence - stimulates transcription

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5
Q

how do transcriptional factors stimulate the transcription of genes?

A

by binding to a specific base sequence in DNA

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6
Q

why can’t transcriptional factors bind to genes that are switched off?

A

the site on the DNA that binds to the transcriptional factors are not active

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7
Q

what determines whether a gene is switched on or off?

A

association of histones

chromatin

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8
Q

how does the association of histones affect whether a gene is turned on or off?

A

histones affect how tightly the DNA can wind around itself, so determining if the genes are accessible or inaccessible

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9
Q

when the association of histones is weak - is the gene switched on or off and why?

A

the DNA is loosely packed so it is accessible to transcriptional factors and the gene is switched on

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10
Q

when the association of histones with DNA is strong - is the gene switched on or off and why?

A

DNA tightly packed around the histones so is inaccessible to transcriptional factors

gene is switched off

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11
Q

what affects the association of histones with DNA?

A

acetylation of histones

methylation of DNA

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12
Q

how does acetylation of histones affect their association with DNA?

A

it affects the overall charge of the histone - which then affects how associated it is with the DNA sequence

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13
Q

what happens when acetyl groups are added to histones?

A

the histones are less associated with DNA

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14
Q

explain how adding acetyl groups to histones can switch on a gene

A

acetyl group added to histone

histone association with DNA decreases

DNA becomes less tightly wrapped

genes become accessible to transcriptional factors

gene switched on

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15
Q

what happens when acetyl groups are removed from histones?

A

the association of histones with DNA increases

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16
Q

explain how deacetylation leads to genes being switched off

A

acetyl group removed from histone

histone association with DNA increases

DNA becomes more tightly wrapped

genes inaccessible to transcriptional factors

gene switched off

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17
Q

what are the ways that methylation can affect whether genes are switched on or off?

A

affecting binding of transcriptional factors

affects rates of deacetylation of histones

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18
Q

during methylation, where is the methyl group added?

A

to a cytosine base of DNA

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19
Q

how does methylation affect the binding of transcriptional factors?

A

increased methylation prevents binding of transcriptional factors

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20
Q

how does methylation affect levels of acetylation of histones?

A

increased methylation induces deacetylation by attracting histones

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21
Q

explain how increased methylation can switch off a gene

A

increased methylation

deacetylation induced

increased association between DNA and histones

DNA more tightly wrapped

genes innaccesible to transcriptional factors

gene switched off

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22
Q

explain how decreased methylation can turn on a gene

A

decreased methylation

increased acetylation

association between DNA and histone decreases

DNA wrapped less tightly

gene more accessible to transcriptional factors

gene switched on

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23
Q

how does chromatin affect whether genes are switched on or off?

A

different forms of chromatin can affect how tightly wound DNA is

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24
Q

what are the types of chromatin that effect whether genes are switched on or off?

A

heterochromatin

euchromatin

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25
Q

what effect does heterochromatin have on DNA?

A

winds DNA in tightly

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26
Q

what effect does euchromatin have on DNA?

A

packs DNA looser

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27
Q

what is the difference between heterochromatin and euchromatin?

A

heterochromatin is a dense form of chromatin

euchromatin lightly packed form

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28
Q

what is epigenetics?

A

where environmental factors cause heritable changes without changing the order of the DNA code

29
Q

what is the epigenome?

A

the tags on DNA wound around histones

30
Q

what does the epigenome determine?

A

the shape of DNA

31
Q

what is significant about the epigenome determining the shape of DNA?

A

the shape keeps inactive genes silenced

32
Q

what is epigenetic silencing?

A

the epigenome keeping inactive genes silenced

33
Q

what is the epigenome’s cellular memory?

A

the epigenome remembers signals it has received throughout its lifetime

34
Q

what is an example of the epigenome being flexible?

A

tags can be changed by the environment

35
Q

what environmental factors can affect the epigenome?

A

diet, stress

36
Q

where does the epigenome receive signals from?

A

other cells in the body

when in the early foetal stage - from mother as well

37
Q

how can epigenetic tags be removed?

A

by radiation

38
Q

what happens if mRNA is destroyed before translation?

A

protein synthesis cannot occur

39
Q

what can cause mRNA to be destroyed before translation?

A

siRNA

40
Q

what is siRNA?

A

small interfering RNA

molecule that stops the translation of mRNA

41
Q

why is siRNA useful?

A

prevents synthesis of proteins from genes that can cause diseases

42
Q

how is siRNA made?

A

an enzyme cuts dsRNA into siRNA

43
Q

how does siRNA prevent mRNA from being translated?

A

siRNA binds with the enzyme used to cut dsRNA into siRNA

siRNA and enzyme bind with complementary bases on mRNA

enzyme cuts mRNA into sections

mRNA can no longer be translated

44
Q

what is dsRNA?

A

double stranded RNA

(synthesized by humans)

45
Q

what genetic factor causes cancer?

A

damage to genes that regulate mitosis and cell cycle

46
Q

compare the growth rates of benign and malignant tumours

A

benign - slow

malignant - quick

47
Q

what is the appearance of nuclei in benign tumours?

A

normal

48
Q

what is the appearance of nuclei in malignant tumours?

A

larger and darker

holding more DNA to divide

49
Q

what is the differentiation of cells in benign tumours?

A

same differentiation of cells as before the tumour grew

50
Q

what is the differentiation of cells in malignant tumours?

A

de-differentiated cells

51
Q

do benign tumours spread?

A

no - due to adhesion molecules keeping the tumour together

52
Q

do malignant tumours spread?

A

yes as they have no adhesion molecules so spread through bloodstream

53
Q

do benign tumours have a capsule around the tumour?

A

yes - surrounding the whole tumour

54
Q

what do malignant tumours contain instead of a capuse?

A

finger-like projections

55
Q

what are the treatments for benign tumours?

A

surgery

56
Q

what are the treatments for malignant tumours?

A

chemotherapy, radiotherapy, surgery

57
Q

what genes can cause cancer?

A

tumour suppressor genes

oncogenes

58
Q

what is the role of a proto-oncogene?

A

to stimulate cell division when growth factors attach to a protein receptor, activating a gene that tells DNA to replicate

59
Q

what happens when a proto-oncogene mutates into an oncogene?

A

oncogene is permanently activated so always stimulating cell to divide regardless of growth factors

receptor protein always activated

may also produce more growth factors

60
Q

can oncogenes be inherited?

A

yes

61
Q

what is the role of tumour supressor genes?

A

slow down cell division

repair DNA mistakes

tells cells when to die (apoptosis)

62
Q

what happens to mutated tumour surpressor genes?

A

become inactivated

63
Q

what is the effect on the cell of mutated tumour supressor genes?

A

most die

some clone to form tumours due to uncontrolled division

64
Q

are tumour supressor genes inherited?

A

not normally, most acquired by mutation

65
Q

how can hypermethylation lead to cancer?

A

hypermethylation occurs in specific region of tumour supressor gene

tumour surpressor gene inactivated

gene switched off

66
Q

how can hypomethylation lead to cancer?

A

hypomethylation of oncogenes, oncogenes more activated

67
Q

what is the role of oestrogen?

A

regulates menstrual cycle

68
Q

why is it more common for women to develop breast cancer after menopause?

A

reduced production of oestrogen in ovaries

fat cells in breasts produce more to compensate

oestrogen can stimulate tumour growth as it is a transcriptional factor

69
Q
A

Biology A2 (15 decks)

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