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BSMS 102 > Theme 3 - DNA and chromosomes > Flashcards

Theme 3 - DNA and chromosomes Flashcards

1
Q

What phase of the cell cycle do cells spend most of their time?

A

interphase

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2
Q

What three things happen in the gap phases?

A

growth, get ready for replication and accumulate ATP

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3
Q

how big are interphase chromosomes?

A

30nm (no unwound but not mitotic)

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4
Q

what is the purpose of 30nm fibre structure in interphase?

A

allows DNA to be replicated/transcribed

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5
Q

what phase does one a single chromatid become two sister chromatids?

A

S phase - DNA replication

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6
Q

what forms at the centromere and what is the function of this?

A

kinetochore - Attaches to spindle microtubules when chromosomes get pulled apart

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7
Q

what is the state of the nuclear membrane in prophase

A

the nuclear membrane is still in tact

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8
Q

what happens to chromosomes in prophase

A

they condense from the 30nm fibre into mitotic chromosomes

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9
Q

in what phase do mitotic spindles starts to form?

A

prophase

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10
Q

at what stage does the nuclear membrane disintegrate and spindle microtubules attach to kinetochores

A

prometaphase

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11
Q

what causes chromosomes to line up on the equator?

A

tension of the pull of the kinetochores by microtubules

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12
Q

what binds sister chromatids together?

A

cohesins

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13
Q

at what stage do cohesins that bind the sister chromatids together disintegrate?

A

anaphase

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14
Q

give another type of microtubule apart from kinetochore microtubules

A

astral microtubules

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15
Q

give two key events of telephone

A

chromosomes have arrived at the poles and the nuclear envelope reforms

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16
Q

how are organelles assigned o each daughter cell in cytokinesis?

A

randomly

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17
Q

what two molecules control the cell cycle

A

cyclins and cyclin dependent kinases

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18
Q

in what phase does p53 check for DNA damage?

A

G1

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19
Q

what phase do most chemotherapy drugs target?

A

S phase

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20
Q

how many base pairs need to be replicated for a cell to divide?

A

6 billion

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21
Q

how many nucleotides are replicated per second?

A

100/s

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22
Q

why does DNA replication run from 5’ to 3’

A

because the strands are polar

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23
Q

why does the semi conservative nature of DNA replication mean that mutations will be passed on?

A

DNA unzips, hydrogen bonds are broken then each strand acts as a template

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24
Q

what end are nucleotides added on to in DNA replication?

A

3’

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25
Q

what bond forms between new nucleotides as they are added to the growing DNA strand in replication?

A

a strong covalent phosphodiester bond

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26
Q

how many origins of replication are there on one DNA strand at any given time?

A

10,000

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27
Q

why is there discontinuous synthesis on the lagging strand in DNA replication?

A

the 3’ end is moving away from the replication fork - creation of Okazaki fragments that are all joined together

28
Q

what is the action of DNA polymerase in DNA replication?

A

adds nucleotides to the growing strand

29
Q

what is the action of DNA helicase in DNA replication?

A

unwinds the DNA

30
Q

what is the action of DNA primase in DNA replication?

A

adds an RNA primer which allows polymerase to bind and move from 5 to 3

31
Q

what is the action of nucleases in DNA replication?

A

remove the RNA primer

32
Q

what is the action of DNA ligase in DNA replication?

A

joins small gaps together

33
Q

what mutation causes Werner syndrome?

A

mutation in a minor DNA helicase (WRN)

34
Q

what is the usual effect of mutations in mitosis or DNA replication genes?

A

lethality

35
Q

what is the incidence of Werner syndrome?

A

1 in 200,000

36
Q

what are the symptoms of Werner syndrome?

A

premature ageing - accumulation of diseases of old age in 40s/50s eg cataracts, atherosclerosis, cancer

37
Q

what underpins the mechanism of Werner syndrome?

A

mutation in DNA helices causes errors in DNA replication and repair - slower replication and more damage is introduced

38
Q

what two mechanisms prevent accumulation of mutations in DNA replication

A

proof reading and excision repair systems

39
Q

how many mistakes per DNA multiplication probably occur?

A

6

40
Q

what is an internal cause of DNA damage?

A

products of normal cell function eg oxygen free radicals

41
Q

what are three external causes of DNA damage?

A

benzene, cigarette smoke and UV/ionising radiation

42
Q

what does DNA nuclease do in excision repair?

A

come in and cuts out the bad base pair region

43
Q

what does DNA polymerase do in excision repair?

A

adds in the correct base once the incorrect one has been removed

44
Q

what does DNA ligase do in excision repair?

A

bandages all the gaps once the correct base has been inserted

45
Q

what enzyme proof reads DNA?

A

DNA polymerase

46
Q

what group does the DNA polymerase detect when nucleotides are in the wrong place?

A

3’ hydroxyl group - if its not where its supposed to be the base is removed by a nuclease

47
Q

Xeroderma pigmentosa is due to a mutation in what?

A

UV repair system

48
Q

what bases are implicated are Xeroderma pigmentosa?

A

two adjacent thymines

49
Q

what is the problem in XP?

A

UV light causes a covalent bond between them to create a dimer which is usually repaired by mechanisms that remove the dimers - XP dont have a UV repair system so this can’t happen

50
Q

what is the implication of XP?

A

children are acutely sensitive to sunlight, hypo/hyper pigmentation and multiple cancers at a young age

51
Q

how frequent are mutations in the population

A

occur <1% of the Time

52
Q

what is a synonymous SNP?

A

causes no change in the amino acid sequence therefore no bearing on the disease state

53
Q

what is a non synonymous SNP?

A

changes the amino acid sequence

54
Q

give three example of monogenic diseases and the type of mutation that causes them

A

sickle cell (substitution), CF (deletion) and Huntingtons (insertion)

55
Q

what type mutation characterises SCA and where is it found?

A

single nucleotide substitution in the beta globin HBB gene (A to T on chromosome 11)

56
Q

what is the incidence of SCA in the UK?

A

12,500

57
Q

what type mutation characterises CF and where is it found?

A

3 base pair deletion (70% patients) on chromosome 7

58
Q

how many cases of CF are there in the UK?

A

9000

59
Q

what is the implication of deletion mutation in the CFTR gene?

A

CFTR channel is not transported correctly or expressed in the right place therefore there is impaired chloride transport

60
Q

what type mutation characterises Huntington’s and where is it found?

A

insertion mutation on the Huntingtin gene on chromosome 4

61
Q

what are the symptoms of huntingtons?

A

uncontrolled muscle movement, loss of memory, depression, difficulty swallowing and speaking

62
Q

what does a mutation in Huntingtin cause?

A

increased numbers of CAG repeats which stick together and is toxic to nerve cells

63
Q

what number of CAG repeats is normal?

A

6 to 35

64
Q

what number of CAG repeats would a carrier of Ht have?

A

36-39

65
Q

what number of CAG repeats would a Ht sufferer have?

A

> 40

66
Q

what essential process becomes a problem when there are more than 36 CAG repeats in Ht?

A

DNA replication

67
Q

what is the incidence of Huntington’s in the uk?

A

7000

BSMS 102 (14 decks)

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