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Foundations Exam 1 > Genome: DNA Structure, Replication, Repair > Flashcards

Genome: DNA Structure, Replication, Repair Flashcards

1
Q

name 2 situations in which DNA recombination occurs

A

chromosome cross-over during meiosis (accidental, but confers genetic diversity)

immunoglobulin gene rearrangement (for antibody diversity)

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2
Q

name the purines and pyrimidines

A

purines: adenine, guanine (2 rings like “pure” wedding rings)

pyrimidines: cytosine and thymine in DNA, cytosine and uracil in RNA (1 ring like a “pie” crust)

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3
Q

describe the important anatomical structural difference between RNA and DNA

A

RNA: hydroxyl (OH) on 2’ C
DNA: hydrogen on 2’ C

hint: DE-oxy-ribose (deoxygenated carbon, now just a hydrogen)

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4
Q

contrast nucleotide and nucleoside

A

nucleoside = base + 5C sugar

nucleotide = base + 5C sugar + phosphate

aka nucleotide = nucleoside + phosphate

therefore, nucleotide may be called nucleoside mono-, di-, or tri-phosphate

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5
Q

what kind of bond links base to 5C sugar in nucleoside

A

N-glycosidic bond (nitrogen atom of base is bonded to hydrogen atom of sugar)

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6
Q

acyclovir is a drug used to treat herpes simplex virus infections. what kind of drug is it?

A

acyclovir: nucleoside analog of deoxyguanosine

converted into a nucleotide and incorporated into DNA during replication but blocks further DNA synthesis

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7
Q

this nucleoside analog of deoxyguanosine is used to treat HSV infection. What is?

A

acyclovir

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8
Q

this nucleoside analog of deoxythymidine is used to treat HIV/AIDS. What is?

A

azidothymidine (AZT), or zidovudine

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9
Q

what is azidothymidine (AZT) used to treat and how does it work

A

AZT (aka zidovudine) is a nucleoside analog of deoxythymidine used to treat HIV/AIDS

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10
Q

what is zidovudine used to treat

A

zidovudine (aka azidothymidine or AZT) is a nucleoside analog of deoxythymidine used to treat HIV/AIDS

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11
Q

what is another name for azidothymidine and what is AZT an analog of

A

AZT = zidovudine = nucleoside analog of deoxythymidine

used to treat HIV/AIDS (halts DNA replication after conversion into nucleotide)

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12
Q

describe the polarity of nucleotide polymerization

A

phosphodiester bonds between 3’ OH on sugar of one nucleotide and 5’ phosphate on another

leaves free 5’ phosphate group and free 3’ hydroxyl group

[3’ hydroxyl is linked to innermost 5’ phosphate]

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13
Q

endonucleases are known as what kind of enzyme

A

endonucleases are restriction enzymes (site-specific cleavage)

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14
Q

fill in these features of DNA:
- most common form is ___
- ____ - handed
- outer _____ backbone
- ____ base pairs per helical turn
- base pairs _____ to axis of symmetry

A

DNA:
- most common is B FORM, which is:
- RIGHT - handed
- outer SUGAR-PHOSPHATE backbone
- 10 base pairs per helical turn
- base pairs PERPENDICULAR to axis of symmetry

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15
Q

what base pairs are most common at the ends of a DNA sequence

A

A=T (2 H bonds) because they are easier to separate than G(3Hbond)C

A=T base pairs are also rich at the origin of replication for the same reason

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16
Q

describe negative supercoils simply (what they are, purpose, etc)

A

negative supercoils = unwinding of helix (fewer helical turns) without breaking any bonds

facilitate strand separation
energetically favored (less tension than relaxed DNA)
make up the tertiary structure of DNA

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17
Q

explain what DNA topoisomerases do

A

enzymes that change tertiary structure of DNA (supercoils)

remove positive supercoils (extra tight winding) ahead of strand opening and excess negative supercoils (opposite direction winding) behind strand opening

have nuclease and ligase activity - transiently break one/both DNA strands, pass other strand through break, and rejoin (to remove one loop, and restore helix)

Topo I cuts single strand, Topo II cuts both strands

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18
Q

what 2 enzymatic functions do DNA topoisomerases have

A

nuclease and ligase activity

(cut strand/s, rejoin them)

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19
Q

this topoisomerase II is found only in prokaryotes and facilitates bacterial DNA replication. what is?

A

DNA gyrase

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20
Q

what kind of drugs block the activity of DNA gyrase, a topo II?
examples include Novobiocin, Nalidixic acid, Ciprofloxacin

A

quinolone drugs

inhibit bacterial DNA synthesis by blocking DNA gyrase (which is only found in prokaryotes)

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21
Q

certain chemotherapeutic drugs target eukaryotic topoisomerases. Examples include Camptothecin, which targets Topo I, and Adriamycin and Etoposide, which target Topo II

how do these work?

A

inhibit ability of topoisomerases to rejoin DNA, converting topoisomerases to DNA breaking agents

cause side effects to any rapidly dividing cells (hair loss, etc)

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22
Q

what are chromatin and nucleosomes comprised of?

A

chromatin = DNA + histones (small basic proteins, rich in Arg and Lys)
[histones: H1, H2A, H2B, H3, H4]

nucleosomes: repeating units of chromatin with DNA spacer in between (bound to histone H1)

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23
Q

what type of interactions hold together DNA double helix supercoils and histones and how many histones are in each nucleosome core?

A

positive/negative charge interactions (negative DNA, positive/basic histones)

histone octamer has 2 molecules each of H2A, H2B, H3, H4

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24
Q

solenoid

A

chromatin wound into helical tubular coil for tighter packaging

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25
Q

after DNA replication is completed, H1 histone binds spacer DNA and nucleosomes pack tightly into ____

A

solenoid (large DNA loops)

solenoid DNA loops coil around a protein scaffold, with loops radiating from scaffold —> creates classic 4 arm structure with 2 chromatids joined by a centromere

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26
Q

which kind of DNA replication occurs from just a single origin:
prokaryotic
eukaryotic

A

prokaryotic DNA is replicated from SINGLE origin

(eukaryotic DNA replicated from many origins)

either way, replication proceeds on both sides of origin in opposite directions (replication fork on each side)

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27
Q

function of DNA helicase

A

binds near replication fork on either side of the origin and catalyzes DNA strand separation

USES ATP to break H bonds

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28
Q

how do inhibitors of HSV helicase-primase work?

A

stabilize interaction of helicase-primase with its viral DNA substrate, inhibiting progression of HSV DNA replication

effect against HSV strains resistant to nucleoside analog therapy (acyclovir)

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29
Q

how are RNA primers created? what direction do they run and what is their function?

A

RNA polymerase (aka primase) synthesizes short RNA primers (~10nt) by copying DNA template strand

RNA primers run 5’—>3’

primers provide free 3’-OH as acceptor of the first deoxyribonucleotide (continuously synthesized on lagging strand)

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30
Q

DNA polymerases copy the ___ strand [don’t overthink it] and use ____________ as precursors

A

DNA polymerases copy TEMPLATE strand, use deoxyribonucleoside triphosphates as precursors

complementary new strand runs 5’-3’, anti parallel to parental strand

DNA pol can ONLY synthesize DNA 5’-3’ direction

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31
Q

leading strands run 5’-3’ [toward/away] replication fork

lagging strands run 5’-3’ [toward/away] replication fork

A

leading strands synthesized continuously TOWARD replication fork

lagging strand synthesized discontinuously AWAY from replication fork (new Okazaki fragments created near replication fork)

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32
Q

in prokaryotes, chain elongation is is catalyzed by….

and how does it work? (specific organic chemistry mechanism)

A

DNA polymerase III: catalyzes chain elongation via NUCLEOPHILIC ATTACK of 3’-OH (growing chain) on innermost 5’-phosphate (incoming deoxyribonucleotide triphosphate), resulting in formation of phosphodiester bond

DNA pol III also has 3’-5’ proofreading activity (backwards reading, exonuclease)

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33
Q

what kind of proofreading activity does prokaryotic DNA Pol III have

A

3’—> 5’ exonuclease activity

removes erroneously introduced nucleotides not complimentary (mismatch repair, MMR)

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34
Q

match the nucleoside analogs with the illness they treat:
analogs: acyclovir, AZT, ddC, gemcitabine, remdesivir
illness: HSV, HIV, cancer, SARS-coV2

A

acyclovir - treats HSV (deoxyguanosine)
AZT - treats HIV (thymidine)
ddC - treats HIV (deoxycytidine)
gemcitabine - treats cancer (deoxycytidine)
remdesivir - treats SARS-coV2 (adenosine)

all prevent elongation in DNA replication

35
Q

DNA Pol III elongates DNA strand in prokaryotes until it is blocked by RNA primer… then what happens?

A

DNA Pol I uses 5’—>3’ exonuclease activity to remove RNA primers from Okazaki fragments, then uses 5’—>3’ polymerase activity to fill in the gap

DNA Pol I then proofreads 3’—>5’ with exonuclease activity (backwards reading)

DNA ligase then joins fragments (ATP DEPENDENT)

a phosphodiester bond is formed between 5’-P on chain made by DNA Pol III and 3’-OH on chain made by DNA Pol I

36
Q

in [prokaryotic/eukaryotic] DNA replication, there are many origins from which replication forks are created on both sides for bidirectional replication

A

eukaryotic - MANY origins
prokaryotic - ONE origin

37
Q

what are the 3 DNA polymerases of eukaryotic replication and their role

A

Pol alpha: synthesizes primers for both leading and lagging strands (primase and polymerase activity)

Pol delta: synthesizes lagging strand (polymerase and exonuclease activity)

Pol epsilon: synthesizes leading strand (polymerase and exonuclease activity)

38
Q

which of these function(s) does eukaryotic Pol alpha have:
primase
polymerase
exonuclease

A

Pol alpha: primase (RNA) and polymerase (DNA) activity

synthesizes short RNA primers, extends primers with DNA

leading and lagging strands

NO exonuclease/proofreading

39
Q

what does Pol delta need to associate with to synthesize the lagging strand of DNA?

A

PCNA: proliferating cell nuclear antigen

[PCNA also associates with Pol epsilon]

40
Q

Pol delta (lagging strand) has 3’-5’ exonuclease activity, and also displaces the 5’ end of primers from Okazaki fragments. What happens to these primer 5’ end?

A

degraded by FEN1 (flap exonuclease)

41
Q

what is the function of FEN1

A

flap exonuclease

degrades primer 5’ ends that are displaced from Okazaki fragments by Pol delta

42
Q

PCNA associates with what DNA polymerase? (specific)

A

PCNA (proliferating cell nuclear antigen) associates with Pol delta (lagging strand, eukaryotic)

AND Pol epsilon (leading strand, eukaryotic)

43
Q

name the two eukaryotic DNA Pols that have 3’-5’ exonuclease proofreading activity

A

Pol delta (lagging) and Pol epsilon (leading)

NOT Pol alpha

44
Q

what happens to nucleosomes/histones during DNA replication?

A

nucleosomes are displaced as replication fork advances

histones remain loosely associated with one parental strand, new histones are synthesized simultaneously with DNA replication

nucleosomes reform behind advancing replication fork

45
Q

telomeres are rich in which nitrogenous base

A

G (triple H bond with C for stability)

46
Q

Without _____, DNA from linear chromosomes would be degraded, recombined, or fuse end-to-end

A

telomere T-loops

47
Q

telomerase:
1. is a _______ complex
2. adds G-rich repeats to the single-stranded _____ ends of linear chromosomes
3. has _____ activity

A

telomerase:
1. ribonucleoprotein (RNA + protein) complex
2. adds G-repeats to ss 3’ ends
3. has reverse transcriptase activity via hTERT (makes DNA from RNA)

48
Q

An autopsy report reveals that a patient suffered bone marrow failure due to loss of hematopoietic renewal. Defects were noted in tissues with rapidly dividing cells: alopecia, leukoplakia (precancerous oral lesions), fibrosis, cirrhosis, and hypogonadism.

Genetic analysis reveals both stem and germ cells had a mutation in the RNA component of telomerase, reducing its activity. What condition does this describe?

A

Dyskeratosis congenita

49
Q

Briefly describe dyskeratosis congenita and its cause

A

defects in tissues with rapidly dividing cells
patients often die from bone marrow failure (loss of hematopoietic renewal)

inherited disease caused by reduced telomerase activity (stem and germ cells affected)

50
Q

what DNA repair mechanism would be utilized following a substitution, insertion, or deletion?

A

mismatch repair (no damage, just wrong pairing)

51
Q

what type of DNA repair is utilized for bulky lesions, photoproducts, or chemical adducts?

A

nucleotide excision

global genomic - for transcriptionally inactive DNA

transcription-coupled - for transcriptionally active DNA (damage halts RNA Pol II along template strand of DNA)

52
Q

how do prokaryotic and eukaryotic cells recognize the strand with the error from the parental strand in mismatch repair (MMR)?

A

prokaryotic: Mut proteins, recognize the new strand lacks methyl groups

eukaryotic: MSH and MLH proteins, unknown mechanism

53
Q

mismatch repair pathway uses a endonuclease or exonuclease to fix base pairing?

A

BOTH:
endonuclease cleaves strand on either side of mismatch

helicase and exonuclease removes DNA between incision and mismatch

DNA Pol III (prokaryotic) or Pol delta/epsilon + PCNA (eukaryotic) fills gap, followed by DNA ligase

54
Q

microsatellite instability (MSI) is a sensitive diagnostic marker for what

A

loss of mismatch repair (MMR) activity in tumors - hallmark of MMR-deficient cells

[microsatellite sequences are short repeats found in non-coding regions, MMR defects most frequent in repetitive DNA tracts]

55
Q

Lynch syndrome is due to a defect in what repair pathway?

A

Lynch syndrome = HNPCC (hereditary nonpolyposis colorectal cancer)… patients at high risk for colorectal cancer, among others

due to defect in mismatch repair (MMR) - most patients have mutation in MSH2 or MLH1 (recognize error strand from parent strand)

microsatellite instability (MSI) is a hallmark, can be tested via PCR

56
Q

oxidation, deamination, depurination, or alkylation of nitrogenous bases caused by ROS, carcinogens, or toxins requires what kind of DNA repair?

A

base excision repair (BER) - for damage to a single base

  1. glycosylase cleaves N-glycosidic bond
  2. apurinic/apyrimidic endonuclease cleaves sugar-phosphate backbone
  3. deoxyribose phosphate lyase removes sugar-phosphate residue
  4. DNA Pol I (beta) fills gap, followed by DNA ligase
57
Q

what enzymes (4) are needed for base excision repair (BER)? What do they do (specific)?

A
  1. glycosylase: cleaves N-glycosidic bond between base/deoxyribose
  2. apurinic/apyrimidic (AP) endonuclease: cleaves sugar-phosphate backbone
  3. deoxyribose phosphate lyase: removes sugar-phosphate residue
  4. DNA Pol I (beta) / DNA ligase: fills gap
58
Q

A 35yo M pt presents with colon cancer. Genetic analysis reveals biallelic mutation in a gene encoding a DNA glycosylase MYH. The pt most likely has defective _____ DNA repair

A

base excision repair (BER)

59
Q

describe Werner’s Syndrome: its hereditary pattern, phenotype, and cause

A

Werner’s Syndrome:
-rare autosomal recessive
-causes premature aging (20-30yo), presents with cataracts, atherosclerosis, cancer, etc
-cells have mutations in DNA helicase WRN which is important for base excision repair (BER) and formation of T-loops

[cells sensitive to ROS, chromosomal rearrangements, and telomere fusions and shortening]

60
Q

A 23yo M pt presents with skin atrophy, cataracts, and atherosclerosis. He is in the 30th % height for his age. Genetic analysis reveals a mutation in the RecQ-family DNA helicase WRN. What is your diagnosis?

A

Werner’s Syndrome: rare autosomal recessive disorder

mutation in base excision repair (BER) pathway —> cells sensitive to ROS and chromosomal rearrangements

61
Q

Ultraviolet light induces ____ formation between _____ in the DNA of skin cells. This leads to distortion of the DNA helix and frame shift mutations. Fortunately, these lesions can be correct by _____

A

Ultraviolet light induces DIMER formation between PYRIMIDINES in the DNA of skin cells. This leads to distortion of the DNA helix and frame shift mutations. Fortunately, these lesions can be correct by NUCLEOTIDE EXCISION REPAIR (NER)

62
Q

Xeroderma pigmentosum (XP) is a hereditary disorder in which patients show extreme solar sensitivity and high risk of skin cancer as well as internal cancers.

XP results from defects in the Global Genomic or Transcription-coupled NER?

A

Global Genomic Nucleotide Excision Repair defect —> XP

mutations in damage recognition or helicase activity

[note: XP can also present with neuronal degeneration depending on which protein is affected]

63
Q

This hereditary developmental and neurological disorder is associated with defects in transcription-coupled NER (TC-NER) which affect recognition of stalled RNA Pol II. Patients present with growth delays, intellectual disabilities, neuron demyelination, and sun sensitivity. However, they do not present with increased risk of skin cancer. What is…

A

Cockayne syndrome

increased risk of cancer is not seen because transcription does not resume after RNA Pol II is blocked - damaged transcriptionally active cells likely undergo apoptosis

64
Q

What is Cockayne syndrome and what causes it?

A

hereditary developmental and neurological disorder associated with defects in TC-NER (transcriptionally coupled nucleotide excision repair)

growth delays, intellectual disabilities, demyelination, sun sensitivity

NOT at higher risk of cancer because transcription does not resume after RNA Pol II is blocked (cancer can’t form)

65
Q

tumor cells deficient in nucleotide excision repair are very sensitive to this chemotherapeutic drug, which forms bulky intra-strand adducts within DNA

A

Cisplatin

66
Q

match:
Global Genomic NER
Transcriptionally Coupled NER
with
neurodegeneration
increased risk of cancer

A

GG-NER —> increased risk of cancer but NOT CNS disorder (used in DNA that is not transcriptionally active)

TC-NER —> neurodegeneration but NOT increased cancer risk (RNA Pol II is stalled and cannot resume, so cancer can’t form)

HOWEVER: GG-NER and TC-NER feed into common pathway, in which mutations can cause an increased risk of cancer AND neurodegeneration

67
Q

loss of a single nucleotide and damaged 5’ and/or 3’ termini at the site of the break is repaired by what mechanism

A

single strand break repair

68
Q

in SSB Repair:
1. ____ recognizes the SSB
2. ____ is recruited as a molecular scaffold
3. ____ processes/fixes the 3’ / 5’ end damage
4. ____ inserts the missing nucleotide
5. DNA ligation

A

SSB:
1. PARP-1
2. XRCC1
3. Aprataxin (APTX)
4. DNA Pol beta

69
Q

this autosomal recessive spinocerebellar ataxia syndrome presents with peripheral neuropathy, hypercholesterolemia, hypoalbuminemia, and cerebellar atrophy. It is caused by a mutation in APTX. What is this condition, and what repair mechanism is deficient?

A

Ataxia Oculomotor Apraxia - deficient in SSB repair pathway

loss of apraTAXin (APTX) gene causes aTAXia [oculomotor] aPRAXia

70
Q

what is the hereditary pattern of Ataxia Oculomotor Apraxia, a disease caused by mutation in Aprataxin (APTX) gene, leading to deficient SSB repair pathway?

A

autosomal recessive

71
Q

contrast the two types of double strand break (DSB) repair

A

non-homologous end-joining (NHEJ):
major pathway, can occur any point in cell cycle, does not require sequence homology, error prone and can lead to chromosomal translocations

homologous recombination (HR):
only S and G2 phase of cell cycle (when sister chromatid is present), requires homology of DNA (undamaged chromosome is template), non-mutagenic

72
Q

what type of DSB repair does this pathway describe?
1. Ku70/Ku80 bind DNA ends
2. frayed ends removed by endonuclease activity of DNA-PKcs:Artemis
3. DNA ligase joins ends

A

NHEJ (non-homologous end joining)

73
Q

why can’t homologous recombination occur at any point in the cell cycle?

A

sister chromatid must be present to use homologous DNA of undamaged chromosome as a template

only S and G2 phase

74
Q

what kind of DNA repair does this pathway describe?
1. RAD52 binds DNA ends
2. RAD51 recombinase searches for sequence homology
2b. BRCA1 and BRCA2 regulate RAD51
3. single strand invasion, nuclease and helicase activation, ligase joins strands

A

homologous recombination (HR) double strand repair

75
Q

BRCA1 and BRCA2 mutations cause susceptibility to breast cancer. However, some chemotherapeutic drugs such as bleomycin (oxidizing agent), camptothecin (topoisomerase I inhibitor), and anthracyclines (Top II inhibitors) may be effective because they induce ____

A

double strand breaks (DSBs)

BRCA1 and BRCA2 regulate RAD51 in homologous recombination DSB repair

76
Q

patients with Ataxia Telangiectasia have increased chromosomal abnormalities in T and B cells and a higher propensity to develop lymphoid cancer. They are hypersensitive to ionizing radiation. What mutation is associated with this disorder and what kind of repair mechanism is faulty?

A

Ataxia Telangiectasia (AT): autosomal recessive, associated with mutation in ATM protein (slows down replication after DSB to allow repair)

faulty double strand break repair

77
Q

A 36yo F pt presents with immune deficiency and lymphoid tumors. Genetic analysis reveals a mutation in the ATM protein. What does this protein do, and what is your diagnosis?

A

ATM: activated by DSB, signals to cell-cycle checkpoint to slow cell cycle for repair
ATM also responds to DNA breaks during B and T development/ differentiation (mutation —> immune deficiency)

diagnosis: Ataxia Telangiectasia (AT) - autosomal recessive

78
Q

T/F: the monomer units in polynucleotide chains are joined together by 3’-5’ phosphodiester bonds

A

TRUE

79
Q

all type II topoisomerases have ___ and ___ activity

A

nuclease and ligase

DNA gyrase is a Top II - can create bubble

80
Q

which of these processes does NOT require DNA Top II?
replication
recombination
repair
transcription

A

none - DNA Top II is required for ALL (replication, recombination, repair, transcription)

DNA Top alter supercoiling, negative supercoils facilitate strand separation, which is required in all of these events

81
Q

A mutation inhibiting the 5’-3’ exonuclease activity of DNA Pol I in a bacteria strain is most likely to cause which of these?
a. increased number of replication errors
b. accumulation of telemeric repeats
c. defect in mismatch repair
d. defect in removal of RNA primers
e. defect in DNA chain elongation

A

d. defect in removal of RNA primers - 5’-3’ exonuclease activity of DNA Pol I removes RNA primers so it can fill gaps

-DNA pol III and I proofread, so not increased number of replication errors
-bacterial DNA is circular, so not telemeric repeats
-DNA Pol III performs mismatch repair (and lagging strand synthesis)

82
Q

nucleoside analog work by suppressing ____

A

DNA chain elongation

nucleoside analog is converted to nucleotide by kinases and incorporated but prevent nucleophilic attack

83
Q

What repair mechanism is used to repair thymine dimers?

A

Nucleotide excision repair

Thymine dimers are source of damage in xeroderma pigmentosum

84
Q

Abasic sites are repaired by what mechanism

A

Base excisison repair - for damage of one nucleotide

Foundations Exam 1 (33 decks)

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