DNA METABOLISM Flashcards

1
Q

the tendency of an organism to
possess the characteristics of its
parent(s)

A

Heredity

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2
Q
  • the elements/units carrying and
    transferring inherited characteristics from parent to offspring
  • contained within the nuclei of cells in association with the chromosomes
A

genes

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3
Q

must be very Blank so that genetic info can be stored in it and transmitted countless times to subsequent generations

A

stable

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4
Q

must be capable of precise copying or Blank so that its info is not lost or altered

A

replication

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5
Q

although stable, must also be subject to change in order to account for the appearance of Blank (short term) and for Blank (long term)

A

mutant forms, evolution

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6
Q

the material of heredity

A

DNA

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7
Q
  • 2 identical copies of the
    original DNA
  • strand separation
  • copying of each strand
  • each separated strand
    acts as a template for
    the synthesis of a new
    complementary strand
A

DNA replication

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8
Q

one completely
new DNA duplex
& the original
DNA duplex

A

Conservative

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9
Q

one parental
strand & one
new strand

A

Semiconservative

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10
Q

each of the 4 strands
contains both newly
synthesized segments &
segments from the
parental strands

A

Dispersive

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11
Q

replication of DNA molecules begins at one or more specific regions called the Blank

A

origin(s) of replication

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12
Q

excepting certain Blank and Blank, proceeds in both directions from this origin

A

bacteriophage chromosomes and plasmids

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13
Q

replication of E. coli DNA begins at
Blank, a unique 245-bp chromosomal site that contains Blank tetranucleotide sequences along its length

A

oriC, 11 GATC

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14
Q
  • involves two replication forks that move in opposite directions
  • predicts that, if radioactively labeled nucleotides are provided as substrates for new DNA synthesis, both replication forks will become radioactively labeled
A

bidirectional replication

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15
Q
  • the enzyme that carries out DNA
    replication
  • uses single-stranded DNA (ssDNA) as a template and makes a complementary strand by polymerizing deoxynucleotides in the order specified by their pairing with bases in the template
A

DNA polymerase

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16
Q

synthesize DNA only in a Blank
direction, reading the antiparallel
template strand in a Blank sense

A

5’→3’, 3’→5’

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17
Q

How does DNA polymerase copy the parent strand that runs in the 5’→3’ direction at the replication fork?

A
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18
Q

because DNA polymerase must read the template
strand in the 3’→ 5’ direction, the 5’→ 3’ parental strand must wrap around in Blank

A

trombone fashion

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19
Q

chain growth is in the Blank & Blank to the template strand

A

5’→ 3’ direction, antiparallel

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20
Q

require a primer Blank w/ a free Blank to initiate DNA synthesis

A

oligonucleotide, 3’-OH

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21
Q

Why primer is essential?

A
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22
Q

Biochemical Characterization of DNA Polymerases DNA polymerases can catalyze the synthesis of DNA if
provided with

A
  • all 4 dNTPs
  • a template DNA strand to copy
  • a primer
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23
Q

the primer must possess a free 3’-OH end to which an incoming
Blank is added

A

deoxynucleoside monophosphate

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24
Q

in vivo, a short Blank is invariably the primer, synthesized by a DNA dependent RNA polymerase activity

A

RNA strand

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25
Q
  • the degree to which a particular DNA polymerase remains associated with the template
A

processivity

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26
Q

are extraordinarily processive

A

replicative DNA polymerases

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27
Q

some DNA polymerases (DNA repair) are only modestly processive, synthesizing a DNA strand only Blank to Blank bases long before falling off

A

3 to 200

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28
Q

The Blank (DNA polymerase III
holoenzyme) can replicate an entire strand of the E. coli chromosome (4.6 mega bases) without falling off

A

E. coli replicative DNA
polymerase

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29
Q

DNA duplex is unwound by the action of DNA Blank and Blank

A

gyrase and helicase

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30
Q

periodically primes synthesis on the lagging strand

A

primase

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31
Q

the single strands are coated with Blank

A

SSB (ssDNA-binding protein)

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32
Q

each half of the dimeric replicative polymerase is a core polymerase
bound to its template strand by a Blank

A

β-subunit sliding clamp

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33
Q

*act downstream on the lagging
strand to remove RNA primers, replace them with DNA, and ligate the Okazaki fragments

A

DNA polymerase I and DNA ligase

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34
Q

the polymerase active site is a Blank, and the 3’-exonuclease activity is an Blank

A

proofreader, editor

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35
Q
  • located diametrically opposite from oriC on the E. coli circular
    chromosome
  • where the oppositely moving
    replication forks meet and
    replication is terminated
A

terminus region (Ter or t) locus

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36
Q
  • act as terminators
A

Ter sequences

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37
Q

clusters of Blank or Blank Ter sequences are organized into 2 sets inversely
oriented with respect to one
another

A

3 or 4

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38
Q

termination requires binding of a
specific replication termination
protein, Blank, Blank

A

Tus protein, to Ter

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39
Q
  • a contrahelicase
  • prevents the DNA duplex from
    unwinding by blocking progression
    of the replication fork
  • inhibit the ATP dependent DnaB
    helicase activity
A

Tus protein

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40
Q

is organized into
chromosomes that are
compartmentalized within the
nucleus

A

eukaryotic DNA

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41
Q

in a dividing human cell, a carefully choreographed replication of Blank of DNA distributed among 46 chromosomes occurs

A

6 billion bp

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42
Q
  • the events associated with cell
    growth and division in eukaryotic
    cells
A

cell cycle

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43
Q
  • longest part of the cell cycle
  • characterized by rapid growth
    and metabolic activity
A

G1 (gap)

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44
Q
  • cells that are quiescent, that is,
    not growing and dividing (such
    as neurons)
A

G0

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45
Q
  • time of DNA synthesis
A

S phase

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46
Q
  • a relatively short period of
    growth when the cell prepares
    for cell division
A

G2

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47
Q

How are the ends of chromosomes replicated?

A
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48
Q
  • specialized structures at the ends of chromosomes
A

telomeres

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49
Q

consist of short (5–8 bp), tandemly
repeated, GC-rich nucleotide
sequences that form protective caps Blank to Blank at the ends of chromosomal DNA

A

1 to 12 kbp long

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50
Q

aid in chromosome maintenance
and stability by protecting against
Blank or Blank

A

DNA degradation or rearrangement

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51
Q

lagging strand synthesis at the 3’
ends of chromosomes is primed by
Blank to form Blank, but these RNA primers
are subsequently removed, resulting
in gaps in the progeny 5’-terminal
strands at each end of the
chromosome after each round of
replication (primer gap)

A

RNA primase, Okazaki
fragments

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52
Q
  • an RNA-dependent DNA
    polymerase which adds telomeres
    to the ends of chromosomal DNA
  • maintains chromosome length by
    restoring telomeres at the 3’-ends
    of chromosomes
A

telomerase

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53
Q

a specialized reverse transcriptase
containing a catalytic subunit

A

✓ TERT (TElomerase Reverse
Transcriptase)

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54
Q

RT, for

A

RNA Template

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55
Q

TER, for

A

TEmplate
containing telomerase RNA

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56
Q

a Blank is created at the 3’-end of each DNA strand

A

G-rich region

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57
Q

a Blank is created at the 5’-end of each DNA strand

A

C-rich region

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58
Q

the Blank serves as the template for the DNA polymerase activity of telomerase

A

ribonucleic acid of human telomerase

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59
Q

in replication of the lagging strand, short RNA
primers are added (pink) and extended by Blank

A

DNA polymerase

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60
Q

the result is a Blank at the 5’-end of each
strand (only one end of a
chromosome)

A

gap (primer gap)

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61
Q

indicate sequences at the
3’-end that cannot be copied by
conventional DNA replication

A

asterisks

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62
Q
  • the G-rich ends of telomeres can
    arrange into four-stranded Blank
A

G quadruplex structures

63
Q

the single-stranded 3’-overhangs at
the telomeric ends of chromosomes
are a hazard because they resemble
Blank

A

Damaged DNA

64
Q
  • a protein complex with 6 distinct
    subunits
  • telomere end-protection protein
A

shelterin

65
Q

How are RNA Genomes Replicated?

A
66
Q
  • noted that inhibitors of DNA
    synthesis prevented infection of
    cells in culture by RNA tumor
    viruses such as avian sarcoma virus
  • noted that inhibitors of DNA synthesis
    prevented infection of cells in culture
    by RNA tumor viruses such as avian
    sarcoma virus
  • proposed that DNA is an intermediate
    in the replication of such viruses
  • an RNA tumor virus can use viral RNA
    as the template for DNA synthesis
A

Howard Temin (1964)

67
Q
  • independently discovered a viral
    enzyme capable of mediating such a
    process
A

Temin and David Baltimore (1970)

68
Q
  • an RNA-directed DNA polymerase
  • synthesizes polynucleotides in the
    5’→ 3’ direction
  • requires a primer
A

reverse transcriptase

69
Q

the primer is a specific Blank
molecule captured by the virion
from the host cell in which it was
produced

A

tRNA

70
Q

the 3’-end of the tRNA is base
paired with the Blank at the site where DNA synthesis initiates

A

viral RNA template

71
Q

reverse transcriptase then
transcribes the RNA template into a
complementary DNA (cDNA) strand
to form a Blank

A

double-stranded DNA:RNA hybrid

72
Q

all RNA tumor viruses contain
reverse transcriptase within their
Blank

A

virions (viral particles)

73
Q
  • RNA viruses that replicate their
    RNA genomes via a DNA
    intermediate
A

retroviruses

74
Q
  • this enzymatic activity creates a ss
    stranded DNA copy of the RNA
    genome of the virus
A

RNA-directed DNA polymerase
activity

75
Q
  • a nuclease that specifically
    degrades RNA chains in DNA:RNA
    hybrids
  • an exonuclease activity that
    degrades the template genomic
    RNA
  • removes the priming tRNA after
    DNA synthesis is completed
A

RNase H activity

76
Q
  • replicates the ssDNA remaining after
    RNase H degradation of the viral
    genome, yielding a DNA duplex
A

DNA-directed DNA polymerase
activity

77
Q

this DNA duplex directs the
remainder of the viral infection
process or becomes integrated into
the host chromosome, where it can lie
dormant for many years as a Blank

A

provirus

78
Q

Blank is of great clinical interest because it is the
enzyme for replication of the AIDS virus

A

HIV reverse transcriptase

79
Q

DNA synthesis by HIV reverse
transcriptase is blocked by
dideoxynucleoside analogs such as
Blank and Blank

A

AZT and 3TC

80
Q

HIV reverse transcriptase
incorporates these analogs into
growing DNA chains in place of
Blank or Blank

A

dTMP (in the case of AZT) or dCMP
(in the case of 3TC)

81
Q

HIV reverse transcriptase is error
prone: It incorporates the wrong base at a frequency of 1 per Blank to Blank
nucleotides polymerized

A

2000 to
4000

82
Q

How is the Genetic Information
Rearranged by Genetic
Recombination?

A
83
Q
  • the natural process by which
    genetic information is rearranged to
    form new associations.
  • genetic recombination is the
    exchange (or incorporation) of one
    DNA sequence with (or into)
    another (molecular level)
A

Genetic recombination

84
Q
  • recombination which involves
    reaction between very similar
    sequences (homologous) of DNA
A

homologous recombination

85
Q
  • incorporation of a DNA segment
    whose sequence differs greatly from
    the DNA at the point of insertion
A

nonhomologous recombination

86
Q
  • is generally used to fix the DNA so that
    information is not lost
A

homologous recombination

87
Q
  • reported the results of her studies on
    an activator gene in corn (Zea mays)
    that was recognizable principally by its
    ability to cause mutations in other
    genes
A

Barbara McClintock(1950)

88
Q

were an internal source of mutation

A

activator genes

89
Q
  • found in all kingdoms of life and
    constitute a significant portion of
    genomes
A

transposons

90
Q

in humans, Blank of the genome is
transposon DNA

A

54%

91
Q

transposons range in size from several hundred
base pairs to more than Blank

A

8 kbp

92
Q
  • enzyme responsible for transposon
    mobility
  • binds to the end of a transposon
A

transposase

93
Q

catalyzes a cut-and-paste
mechanism that inserts the
transposon into a chromosome or
remobilizes the transposon to a
different location in the genome →
Blank

A

transposition events

94
Q
  • the smallest transposons
  • insert apparently at random in the
    genome
A

insertion sequences (Iss)

95
Q

is a major force in
evolution because transposition
events can move genes to new
places or lead to the duplication of
existing genes

A

transposition

96
Q

are susceptible to chemical alterations
that arise from environmental
damage or errors during synthesis

A

biological macromolecules

97
Q

for RNAs, proteins, or other cellular
molecules, most consequences of
such damage are avoided by
replacement of these molecules
through Blank

A

normal turnover (synthesis
and degradation)

98
Q

is vital to cell
survival and reproduction.
* its information content must be
protected over the life span of the cell
and preserved from generation to
generation

A

the integrity of DNA

99
Q
  1. high-fidelity replication systems
  2. repair systems that correct DNA
    damage that might alter its information
    content
A

Safe guards

100
Q
  • the nucleotide sequence in one
    strand is directly related to the
    sequence in the other
    DNA damage may arise from Blank and Blank
A
  • endogenous processes
  • exogenous processes
101
Q
  • chemical reactions (oxidation,
    alkylation, or deamination of bases)
  • loss of bases due to cleavage of N
    glycosidic bonds
A

Endogenous processes

102
Q

What are the examples of exogenous agents?

A
  • UV light
  • ionizing radiation
  • mutagenic chemicals
103
Q

Ways in which exogenous agents can
damage DNA

-UV-induced free-radical generation
and crosslinking of adjacent
Blank

A

pyrimidines

104
Q

breakage of the polynucleotide
backbone by Blank

A

ionizing radiation

105
Q

base modifications through

A

chemical reactions

106
Q
  • the human genome has Blank or so
    genes associated with DNA repair
A

150

107
Q

to remove methyl groups from chemically
modified bases

A

methyltransferases

108
Q

, which repairs thymine
dimers

A

photolyase

109
Q

single-strand damage repair relies
on the intact Blank
to guide repair

A

complementary strand

110
Q

Systems repairing this sort of DNA
damage include

A
  • mismatch repair (MMR)
  • base excision repair (BER)
  • nucleotide excision repair (NER)
111
Q
  • the most dangerous form of DNA
    damage
A

Double-Strand DNA Breaks (DSBs)

112
Q

can always provide a
homologous dsDNA, but so can haploid
cells such as bacteria, if the break
occurs when such cells are transiently
diploid, as they are during replication

A

diploid cells

113
Q

DSBs are common in eukaryotic
cells; estimates suggest a frequency
of Blank DSBs per cell per day

A

10

114
Q

2 most prominent pathways of DSB
repair are

A
  • nonhomologous DNA end-joining
    (NHEJ)
  • homologous recombination (HR)
115
Q
  • the broken ends at the break site
    are rejoined
  • the lack of a proper DNA template
    means that NHEJ is error-prone
A

NHEJ

116
Q

DSBs that arise as the cell progresses from S into G2 during
the cell cycle can be repaired through Blank

A

homologous recombination

117
Q

human DNA replication has an error rate of about Blank mistakes during
copying of the 6 billion base pairs in
the diploid human genome

A

3 bp

118
Q

about Blank (mostly purines) are
lost per cell per day from spontaneous
breakdown in human DNA

A

104 bases

119
Q
  • corrects errors introduced when
    DNA is replicated
  • scans newly synthesized DNA for
    mispaired bases, excises the
    mismatched region, and then
    replaces it by DNA polymerase
    mediated local replication
A

mismatch repair system

120
Q

, often an identifying
and characteristic feature of a
prokaryote’s DNA, occurs just after DNA
replication

A

DNA methylation

121
Q

when the methyl-directed
mismatch repair system encounters
a mismatched base pair, it searches
along the DNA until it finds a Blank

A

methylated base

122
Q

mismatch repair does this by using
an Blank to cut the new,
unmethylated strand and an
Blank to remove the
mismatched bases, creating a gap in
the newly synthesized strand

A

endonuclease, exonuclease

123
Q

Blank
then fills in the gap, using the
methylated strand as template

A

DNA polymerase III holoenzyme

124
Q

Blank reseals the strand

A

DNA ligase

125
Q

the bases in DNA are Blank

A

electron-rich

126
Q

absorption of UV light can lead to formation of Blank if 2 T residues are next to one another

A

thymine dimers

127
Q

these dimers disrupt the information transfer reactions
implicit to Blank and
Blank

A

transcription, translation

128
Q

promotes the
formation of covalent bonds between adjacent thymine residues
in a DNA strand, creating a
Blank

A

UV irradiation, cyclobutyl ring

129
Q

a FAD-dependent enzyme, binds at the
dimer and uses the energy of visible light
to break the cyclobutyl ring, restoring
the pyrimidines to their original form

A

photolyase (photoreactivating enzyme),

130
Q
  • acts on single bases that have been
    damaged through oxidation or other
    chemical modifications during normal
    cellular processes
A

base excision repair

131
Q
  • recognizes and repairs larger regions of damaged DNA
A

nucleotide excision repair (NER)

132
Q
  • consists of more than 30 proteins
    engaged in DNA damage verification,
    excision, gap filling, and ligation
A

NER pathway in humans

133
Q

an oligonucleotide stretch Blank to blank units long is removed

A

27 to 29

134
Q

the resultant gap is then filled in using
DNA polymerase (DNA polymerase I in
prokaryotes or DNA polymerase d or e
and PCNA plus RFC in eukaryotes), and
the sugar–phosphate backbone is co
valently closed by Blank

A

DNA ligase

134
Q

such lesions are recognized by Blank, an inherited human syndrome whose
victims suffer serious skin lesions if
exposed to sun light

A

XPA
protein (xeroderma pigmentosum)

135
Q
  • a DNA-binding dimer of 31-kDa
    subunits
  • verifies that DNA damage has
    occurred
  • serves as a platform for recruitment
    of other NER factors to the damaged
    strand through protein–protein
    interactions
A

XPA

136
Q

What is the Molecular Basis of Mutation?

A
137
Q
  • substitution of one base pair for
    another
  • when a base pairs with an
    inappropriate partner
  • introduction of base analogs into DNA
  • chemical mutagens
A

point mutations

138
Q
  • insertion or deletion of one or
    more base pairs
A

insertions and deletions

139
Q
  • one purine (or pyrimidine) is
    replaced by another
A

transitions

140
Q
  • a purine is substituted for a
    pyrimidine, or vice versa
  • proofreading mechanisms
    operating during DNA replication
    catch most mispairings
A

transversions

141
Q

the frequency of spontaneous
mutation in prokaryotes and
eukaryotes (including humans) is
about Blank base pair per generation

A

10-8 per

142
Q
  • become incorporated into DNA and
    induce mutations through changes
    in base-pairing possibilities
  • 5-bromouracil (5-BU)
  • 2-aminopurine (2-AP)
A

base analogs

143
Q
  • a thymine analog
  • becomes inserted into DNA at sites
    normally occupied by T
A

5-bromouracil

144
Q

less often, 5-BU is inserted into
DNA at Blank, not T sites

A

cytosine sites

145
Q
  • an adenine analog that arises in situ
    in DNA through oxidative deamination
    of A
  • base pairs with cytosine, creating an
    A–T to G–C transition
A

hypoxanthine

145
Q
  • agents that chemically modify
    bases so that their base-pairing
    characteristics are altered
A

chemical mutagens

145
Q

causes the oxidative
deamination of primary amine
groups in adenine and cytosine

A

HNO2

146
Q
  • alkylation of reactive sites on the
    bases to add methyl or ethyl groups
    alters their H bonding and hence
    base pairing
A

alkylating agents

147
Q

nitrosoamines are mutagenic in 2 ways
* they can react to yield Blank
* they can act as Blank

A

HNO2, alkylating agents

148
Q

is a very potent mutagen used in
laboratories to induce mutations in experimental
organisms such as Drosophila melanogaster

A

nitrosoguanidine, N-methyl-N’-nitro-N
nitrosoguanidine

149
Q
  • the addition or removal of one or
    more base pairs leads to insertion or
    deletion mutations, respectively
A

Insertions and Deletions

150
Q
  • misincorporation of all subsequent
    AA in the protein encoded by the
    gene
A

frameshift mutations