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Life Science 3 > Lecture 11 > Flashcards

Lecture 11 Flashcards

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1
Q

Point mutations is a – level base substitution

A

DNA

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2
Q

replace DNA base with the same chemical property

purine–> purine

A

transitions

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3
Q

replace DNA base from different chemical
property
purine –> pyrimidine

A

transversions

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4
Q

one or more DNA nucleotides are added

A

base insertions

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5
Q

one or more DNA nucleotides are deleted

A

base deletions

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6
Q

Base substitutions in coding regions is – level

A

amino acid

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7
Q

change mRNA nucleotide but same aa

A

silent mutation

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8
Q

change mRNA nucleotide change aa

A

missense mutation

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9
Q

change mRNA nucleotide –> stop codon

A

nonsense mutation

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10
Q

altered aa is in the same aa group

A

conservative missense mutation

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11
Q

altered aa is in a different aa group

A

non-conservative missense mutation

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12
Q

DNA damage is unavoidable and arise by – of chemical bonds in DNA

A

spontaneous cleavage

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13
Q

DNA damage can occur via – chemicals in the environment

A

genotoxic

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14
Q

DNA damage can occur via certain by-products of normal –

A

cellular metabolism

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15
Q

DNA damage can occur via environmental agents such as – and -

A

UV light and ionizing radiation

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16
Q

DNA damage can occur via – induced by DNA pol during replication

A

copying errors

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17
Q

inside the cell is - environment

A

reducing

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18
Q

deamination of a cytosine base, converts it into a

A

uracil

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19
Q

deamination of a common modified base 5-methyl cytosine, converts it to a –

A

thymine

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20
Q

depurination can release – and – from a DNA strand

A

guanine and adenine

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21
Q

depurination can a – mutation

A

deletion

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22
Q

common type of damage caused by UV light

A

thymine dimers

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23
Q

thymine dimers interfere with – and –

A

DNA replication and RNA transcription

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24
Q

cells use – to fix DNA regions containing chemically modified bases that distort the normal shape of DNA locally

A

nucleotide excision repair

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25
Q

determine potential mutagens

A

Ames test

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26
Q

base analog of thymine that can bind with guanine

A

5-bromouracil (enol tautomer)

27
Q

intercalating agents that can cause mutations include

A

proflavin, ehtidium, and acridine orange

28
Q

first line of defense in preventing mutations is

A

DNA polymerase

29
Q

proofreading depend on the – of some DNA pol

A

3’–> 5’ exonuclease activity

30
Q

when an incorrect base is incorporated during DNA synthesis, the 3’ end is transferred to the – where the incorrect misfired base is removed

A

exonuclease site

31
Q

– methylates A residues of 5’GATC3’ sequence

A

E. coil dam methylase

32
Q

methylation marks the – therefore the mismatch repair system can distinguish the newly synthesized strands

A

template strands

33
Q

– enables replication to proceed across DNA damage

A

translesion DNA synthesis

34
Q

in photoreactivation, – breaks thymine dimers

A

DNA photolyase

35
Q

methyl group removal by – is an example of direct reversal of DNA damage

A

methlytransferase

36
Q

besides DNA pol, cells have other repair systems called – for preventing mutations due to copying errors and exposure to mutagens

A

DNA excision-repair systems

37
Q

many cancers arise from a loss of one of –

A

DNA repair systems

38
Q

base excision repair removes damaged bases by a specific

A

glycosylase

39
Q

Because a G-T mismatch is almost always caused by a chemical conversion (deamination) – the repair system “knows” to remove the – and replace it with –

A

5-methyl C –> T

remove T and replace with C

40
Q

– is recognized by a DNA glycosylase and flips out the thymine base out of the helix cuts it away from the sugar-phosphate backbone

A

G-T mismatch

41
Q

– an endonuclease specific for the 5’ end of the baseless site cuts the DNA backbone

A

APEI

42
Q

another endonuclease called – which is associated with DNA pol beta removes the deoxyribose phosphate

A

AP lyase

43
Q

– fill the gaps which are sealed by DNA in base excision repair systems

A

DNA pol beta

44
Q

in nucleotide excision repair, a complex of – and – proteins slide along the surface of a double stranded DNA molecule looking for any distortions of the double helix.

A

XP-C and 23B

45
Q

complex of XP-C and 23B recruits then recruits the general transcription factor –, whose helicase subunits partially unwind the double helix.

A

TFIIH

46
Q

After TFIIH is recruited, – then bind to the complex and further unwind and stabilize the helix until a bubble of ~25 bases is formed.

A

XP-G and RPA proteins

47
Q

After a bubble is formed, –(now acting as an endonuclease) and –, a second nuclease, cut the damaged strand on each side of the lesion.

A

XP-G and XP-F

48
Q

during nucleotide excision repair, the DNA fragment with damaged bases is released and –

A

degraded to mononucleotides

49
Q

Lastly, the gap is filled by –, and the remaining nick is sealed by DNA ligase during nucleotide excision repair

A

DNA polymeraseδ/ε

50
Q

error – homologous recombination

A

free

51
Q

error – DNA end joining

A

prone

52
Q

error- free homologous recombination: double strand DNA break forms in the –

A

chromatids

53
Q

error-free homologous recombination: double strand break activates – which leads to the activation of a set of exonucleases that remove nucleotides at the break creating single-stranded 3’ ends

A

ATM kinase

54
Q

error-free homologous recombination: in a BRCA1 and BRCA2 dependent process, – polymerizes on single-stranded DNA with free 3’ ends to form a nucleoprotein filament

A

RAD51

55
Q

error-free homologous recombination: – conducts a homology search on the duplex DNA sequence in the sitter chromatid

A

RAD51 nucleoprotein filament

56
Q

after finding a homology, the RAD51 nucleoprotein filament invades the duplex to form a – in which the single-stranded 3’ end is base-paired to the complementary strand on the homologous DNA strand.

A

joint molecule

57
Q

error-free homologous recombination: DNA pol elongates the 3’ end of the – (using the complementary sequences on the sister chromatid as a template)

A

damaged DNA

58
Q

error-free homologous recombination: When sufficiently long, this repaired 3’ end of the damaged DNA – with the single-stranded end of the other damaged strand.

A

pairs

59
Q

error-free homologous recombination: Any remaining gaps are filled in by DNA polymerase and DNA ligase, regenerating a – double helix in which an entire segment has been regenerated.

A

wild-type

60
Q

The predominant mechanism of double-strand break repair in multicellular organisms.

A

error-prone repair by enjoining

61
Q

error-prone repair by enjoining: nvolves rejoining the – of two DNA molecules.

A

nonhomologous ends

62
Q

error-prone repair by enjoining: Even if joined DNA fragments come from the same chromosome, the repair process results in loss of several base pairs at –(mutations).

A

the joining point

63
Q

error-prone repair by enjoining: -Sometimes broken ends from different chromosomes are accidentally joined together, leading to – of pieces of DNA from one chromosome to another.

A

translocation

Life Science 3 (20 decks)

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